Phenotypes associated with this allele

• Allele Symbol: Trp53^tm1Tyj
• Allele Name: targeted mutation 1, Tyler Jacks
• Allele ID: MGI:1857263
• Summary: 286 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Trp53^tm1Tyj/Trp53^tm1Tyj	129S6.129-Trp53^tm1Tyj Rb1^tm1.1Jyjw	MGI:3769499
hm2	Trp53^tm1Tyj/Trp53^tm1Tyj	129-Trp53^tm1Tyj/J	MGI:3849871
hm3	Trp53^tm1Tyj/Trp53^tm1Tyj	B6.129S2-Trp53^tm1Tyj/J	MGI:3849876
hm4	Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129 * 129S2/SvPas * C57BL/6J	MGI:7484074
hm5	Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas	MGI:3584474
hm6	Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J	MGI:3616345
hm7	Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * BALB/c	MGI:3695127
hm8	Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:2174782
hm9	Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * CBA	MGI:5751693
hm10	Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * FVB/N	MGI:5688516
hm11	Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * FVB/N	MGI:4420446
ht12	Trp53^tm1Tyj/Trp53^+	involves: 129 * 129S2/SvPas * C57BL/6J	MGI:7484082
ht13	Trp53^tm1Tyj/Trp53^+	involves: 129P2/OlaHsd * 129S2/SvPas * BALB/c * C57BL/6	MGI:3818474
ht14	Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas	MGI:3584473
ht15	Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * BALB/cJ * C57BL/6	MGI:5463925
ht16	Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6	MGI:2174783
ht17	Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6 * CBA	MGI:5751694
ht18	Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6 * FVB/N	MGI:5688517
ht19	Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6J	MGI:3629208
ht20	Trp53^tm1Tyj/Trp53^tm2.1Tyj	involves: 129S2/SvPas * 129S4/SvJae	MGI:3584464
ht21	Trp53^tm1Tyj/Trp53^tm3.1Tyj	involves: 129S2/SvPas * 129S4/SvJae	MGI:3584471
ht22	Trp53^tm1Tyj/Trp53^tm1.1Umol	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * C57BL/6NTac	MGI:5790354
ht23	Trp53^tm1Tyj/Trp53^tm2.1Umol	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * C57BL/6NTac	MGI:5790358
ht24	Trp53^tm1Tyj/Trp53^tm3.1Glo	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6	MGI:3722619
cn25	Trp53^tm1Tyj/Trp53^tm1.1Dgk	involves: 129S * 129X1/SvJ * C57BL/6	MGI:5306614
cn26	Telo2^tm1Tdl/Telo2^tm1.1Tdl Trp53^tm1Tyj/Trp53^tm1Tyj Gt(ROSA)26Sor^tm1(cre/ERT)Nat/Gt(ROSA)26Sor^+	involves: 129 * 129P2/OlaHsd * 129S2/SvPas * C57BL/6J	MGI:3819400
cn27	Gt(ROSA)26Sor^tm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sor^tm1(cre/ERT)Nat Trp53^tm1Tyj/Trp53^+	involves: 129 * 129S2/SvPas * C57BL/6	MGI:4443108
cn28	Gt(ROSA)26Sor^tm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sor^tm1(cre/ERT)Nat Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129 * 129S2/SvPas * C57BL/6	MGI:4443109
cn29	Gnl3^tm2.1Rylt/Gnl3^tm2.1Rylt Trp53^tm1Tyj/Trp53^tm1Tyj Tg(CAG-cre/Esr1*)5Amc/0	involves: 129 * 129S2/SvPas * C57BL/6 * CBA	MGI:5523425
cn30	Terf1^tm1.1Blas/Terf1^tm1.1Blas Tg(KRT5-cre)1Tak/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129 * C3H * C57BL/6 * SJL	MGI:4357787
cn31	Cops5^tm1Rpar/Cops5^tm1Rpar Tg(Lck-cre)548Jxm/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129 * C57BL/6 * CBA * SJL	MGI:3783542
cn32	Rps6^tm1Gtho/Rps6^+ Trp53^tm1Tyj/Trp53^tm1Tyj Tg(KRT5-cre)5132Jlj/0	involves: 129 * C57BL/6J * DBA/2J	MGI:6260011
cn33	Rps6^tm1Gtho/Rps6^+ Trp53^tm1Tyj/Trp53^+ Tg(KRT5-cre)5132Jlj/0	involves: 129 * C57BL/6J * DBA/2J	MGI:6260013
cn34	Brca2^tm1Brn/Brca2^tm1Brn Ptch1^tm1Mps/Ptch1^+ Trp53^tm1Tyj/Trp53^+ Tg(Nes-cre)1Kln/0	involves: 129 * C57BL/6 * SJL	MGI:3831342
cn35	Brca2^tm1Brn/Brca2^tm1Brn Ptch1^tm1Mps/Ptch1^+ Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Nes-cre)1Kln/0	involves: 129 * C57BL/6 * SJL	MGI:3831343
cn36	Cdkn2c^tm1Bbd/Cdkn2c^tm1Bbd Trp53^tm1Brn/Trp53^tm1Tyj Tg(Nes-cre)1Kln/0	involves: 129P2/OlaHsd * 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL	MGI:3710322
cn37	Nle1^tm1Cba/Nle1^tm1.1Cota Gt(ROSA)26Sor^tm2(cre/ERT2)Brn/Gt(ROSA)26Sor^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas	MGI:5553372
cn38	Kras^tm4Tyj/Kras^+ Map2k7^tm1.1Twad/Map2k7^tm1.2Twad Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6	MGI:4948964
cn39	Fbxw7^tm1Kei/Fbxw7^tm1Kei Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Lck-cre)1Cwi/?	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:3767597
cn40	Atrip^tm1.1Pof/Atrip^tm1.1Pof Tg(Pax6-cre,GFP)2Pgr/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:6505488
cn41	Nop53^tm2.1Asuz/Nop53^tm2.1Asuz Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Lck-cre)#Jxm/0	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * CBA	MGI:5906184
cn42	Trp53^tm1Brn/Trp53^tm1Tyj Tg(Nes-cre)1Kln/0	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL	MGI:3710323
cn43	Ddb1^tm1Spg/Ddb1^tm1Spg Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Nes-cre)1Kln/0	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL	MGI:3698834
cn44	Brca2^tm1Brn/Brca2^tm1Brn Trp53^tm1Tyj/Trp53^+ Tg(Nes-cre)1Kln/0	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL	MGI:3831340
cn45	Brca2^tm1Brn/Brca2^tm1Brn Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Nes-cre)1Kln/0	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL	MGI:3831341
cn46	Rb1^tm1Tyj/Rb1^tm2Brn Rbl1^tm1Tyj/Rbl1^tm1Tyj Trp53^tm1Brn/Trp53^tm1Tyj Tg(Chx10-EGFP/cre,-ALPP)2Clc/0	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL	MGI:3710239
cn47	Mdm4^tm2Glo/Mdm4^tm2.1Glo Tg(Myh6-cre)2182Mds/0 Trp53^tm1Tyj/Trp53^tm1Brn	involves: 129P2/OlaHsd * 129S/Sv * C57BL/6J * FVB/N	MGI:5907135
cn48	Nf1^tm1Par/Nf1^+ Pten^tm1Hwu/Pten^+ Trp53^tm1Tyj/Trp53^+ Tg(GFAP-cre)25Mes/0	involves: 129S1/Sv * 129S2/SvPas * 129S4/SvJae * 129X1/SvJ * FVB/N	MGI:4840094
cn49	Taf1b^tm1c(EUCOMM)Hmgu/Taf1b^tm1c(EUCOMM)Hmgu Trp53^tm1Tyj/Trp53^tm1Tyj Gt(ROSA)26Sor^tm1(cre/ERT)Nat/Gt(ROSA)26Sor^tm1(cre/ERT)Nat	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6J * C57BL/6N	MGI:6887493
cn50	Gt(ROSA)26Sor^tm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor^+ Ptf1a^tm1.1(cre)Cvw/Ptf1a^+ Tg(tetO-Kras2)12Hev/0 Trp53^tm1Tyj/Trp53^+	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6J * FVB/N	MGI:5569005
cn51	Nf1^tm1Par/Nf1^+ Trp53^tm1Tyj/Trp53^+ Tg(GFAP-cre)25Mes/0	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * FVB/N	MGI:4840090
cn52	Lig4^tm1Pmc/Lig4^tm1Pmc Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Nes-cre)1Kln/0	involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL	MGI:3831348
cn53	Trp53^tm1Tyj/Trp53^tm1Tyj Xrcc2^tm2Pmc/Xrcc2^tm2Pmc Tg(Nes-cre)1Kln/0	involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL	MGI:3831338
cn54	Xrcc1^tm1Pmc/Xrcc1^tm1Pmc Trp53^tm1Tyj/Trp53^+ Tg(Nes-cre)1Kln/0	involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL	MGI:4359665
cn55	Lig4^tm1Pmc/Lig4^tm1Pmc Trp53^tm1Tyj/Trp53^tm1Tyj Xrcc2^tm2Pmc/Xrcc2^tm2Pmc Tg(Nes-cre)1Kln/0	involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL	MGI:3831351
cn56	Xrcc1^tm1Pmc/Xrcc1^tm1Pmc Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Nes-cre)1Kln/0	involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL	MGI:4359666
cn57	Lig4^tm1Pmc/Lig4^tm1Pmc Trp53^tm1Tyj/Trp53^+ Xrcc2^tm2Pmc/Xrcc2^tm2Pmc Tg(Nes-cre)1Kln/0	involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL	MGI:3831355
cn58	Gt(ROSA)26Sor^tm1(cre/ERT2)Tyj/Gt(ROSA)26Sor^+ Tacc3^tm1.1Tno/Tacc3^tm1.2Tno Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S4/SvJae * C57BL/6	MGI:5305073
cn59	Gt(ROSA)26Sor^tm1(cre/ERT2)Tyj/Gt(ROSA)26Sor^+ Tacc3^tm1.1Tno/Tacc3^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S4/SvJae * C57BL/6	MGI:5305074
cn60	Pten^tm1Hwu/Pten^tm1Hwu Tg(Pdx1-cre)89.1Dam/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 * CBA	MGI:4836239
cn61	Trp53^tm1Elee/Trp53^tm1Tyj Tg(GFAP-cre)25Mes/0	involves: 129S2/SvPas * 129S4/SvJae * FVB/N	MGI:3849178
cn62	Rb1^tm3Tyj/Rb1^tm3Tyj Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Nes-cre)1Atp/0	involves: 129S2/SvPas * 129S4/SvJae * FVB/N	MGI:3783529
cn63	Mdm4^tm2Glo/Mdm4^tm2.1Glo Tg(Myh6-cre)2182Mds/0 Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S4/SvJaeSor * 129S7/SvEvBrd * C57BL/6J * FVB/N	MGI:5907132
cn64	Trp53^tm1Tyj/Trp53^tm1Tyj Usp7^tm2Wgu/Usp7^tm2Wgu Tg(Nes-cre)1Kln/0	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * SJL	MGI:5526849
cn65	Mdm2^tm1Glo/Mdm2^tm2.1Glo Tg(Myh6-cre)2182Mds/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd * FVB/N	MGI:3616710
cn66	Tg(Atoh1-sb11)1Mtay/0 TgTn(sb-T2/Onc3)12740Njen/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C3H * C57BL/6J * ICR	MGI:5317026
cn67	Alb^tm1(cre/ERT2)Mtz/Alb^+ Polr2m^tm1.1Rgr/Polr2m^tm1.1Rgr Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:6515759
cn68	Polr2m^tm1.1Rgr/Polr2m^tm1.1Rgr Speer6-ps1^Tg(Alb-cre)21Mgn/Speer6-ps1^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * DBA	MGI:6515760
cn69	Tg(EIIa-cre)C5379Lmgd/0 Tg(Rnu6-RNAi:Bccip)4Zshn/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * FVB/N	MGI:5292118
cn70	Tg(ACTB-NOTCH1)1Shn/0 Tg(Nes-cre)1Kln/0 Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6J	MGI:3044602
cn71	Tg(ACTB-NOTCH1)1Shn/0 Tg(Nes-cre)1Kln/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6J	MGI:3044601
cn72	Kdm6a^tm1Cdcn/Y Tg(CAG-cre/Esr1*)5Amc/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6J * CBA * FVB/N	MGI:6192377
cn73	Trp53^tm1Tyj/Trp53^tm1Tyj Riok2^tm1c(KOMP)Wtsi/Riok2^+ Commd10^Tg(Vav1-icre)A2Kio/Commd10^+	involves: 129S2/SvPas * C57BL/6N * C57BL/10 * CBA/Ca	MGI:6712734
cn74	Rpap3^tm1c(KOMP)Wtsi/Rpap3^tm1c(KOMP)Wtsi Tg(Vil1-cre/ERT2)23Syr/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6N * DBA/2	MGI:7310427
cn75	Atr^tm2Bal/Atr^tm2Bal Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Nes-cre)1Kln/0	involves: 129S2/SvPas * C57BL/6 * SJL	MGI:5316227
cx76	Rb1^tm1.1Jyjw/Rb1^tm1.1Jyjw Trp53^tm1Tyj/Trp53^tm1Tyj	129S6.129-Trp53^tm1Tyj Rb1^tm1.1Jyjw	MGI:3769498
cx77	Nf1^tm1Tyj/Nf1^+ Trp53^tm1Tyj/Trp53^+	B6.129S2-Trp53^tm1Tyj Nf1^tm1Tyj/+ +	MGI:5286078
cx78	Espl1^Gt(XL058)Byg/Espl1^+ Trp53^tm1Tyj/Trp53^+	B6.129-Trp53^tm1Tyj Espl1^Gt(XL058)Byg	MGI:5285701
cx79	Espl1^Gt(XL058)Byg/Espl1^+ Trp53^tm1Tyj/Trp53^tm1Tyj	B6.129-Trp53^tm1Tyj Espl1^Gt(XL058)Byg	MGI:5285700
cx80	Rpl27a^Sfa/Rpl27a^+ Trp53^tm1Tyj/Trp53^+	B6.Cg-Rpl27a^Sfa Trp53^tm1Tyj	MGI:5140357
cx81	Tert^tm1Rdp/Tert^tm1Rdp Trp53^tm1Tyj/Trp53^+	B6.Cg-Trp53^tm1Tyj Tert^tm1Rdp	MGI:3639948
cx82	Nf1^tm1Tyj/Nf1^+ Trp53^tm1Tyj/Trp53^+	(C3H/HeJ x B6.129S2-Trp53^tm1Tyj Nf1^tm1Tyj/+ +)F1	MGI:5286079
cx83	Nf1^tm1Tyj/Nf1^+ Trp53^tm1Tyj/Trp53^+	(CAST/EiJ x B6.129S2-Trp53^tm1Tyj Nf1^tm1Tyj/+ +)F1	MGI:5286080
cx84	Nf1^tm1Tyj/Nf1^+ Trp53^tm1Tyj/Trp53^+	(CBA/J x B6.129S2-Trp53^tm1Tyj Nf1^tm1Tyj/+ +)F1	MGI:5286081
cx85	Lig4^tm1Icrf/Lig4^tm1Icrf Trp53^tm1Tyj/Trp53^tm1Tyj	either: (involves: 129P2/OlaHsd * 129S2/SvPas) or (involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ)	MGI:3655296
cx86	Lig4^tm1Icrf/Lig4^tm1Icrf Trp53^tm1Tyj/Trp53^+	either: (involves: 129P2/OlaHsd * 129S2/SvPas) or (involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ)	MGI:3655297
cx87	Ccne1^tm1Jro/? Trp53^tm1Tyj/Trp53^tm1Tyj	either: (involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6J) or (involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6 * C57BL/6J)	MGI:3586556
cx88	Trp53^tm1Tyj/Trp53^tm1Tyj Trp63^tm1.1Elrf/Trp63^tm1.1Elrf	either: (involves: 129S2/SvPas * C57BL/6 * FVB/N) or (involves: 129S2/SvPas * 129S4/SvJae * 129S6/SvEvTac * C57BL/6)	MGI:4355557
cx89	Nhej1^tm1Fwa/Nhej1^tm1Fwa Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129	MGI:3809981
cx90	Ptch1^tm1Mps/Ptch1^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129 * 129S2/SvPas * C57BL/6	MGI:3759458
cx91	Ptprz1^tm1Schl/Ptprz1^tm1Schl Trp53^tm1Tyj/Trp53^+	involves: 129 * 129S2/SvPas * C57BL/6J	MGI:7484076
cx92	Ptprz1^tm1Schl/Ptprz1^+ Trp53^tm1Tyj/Trp53^+	involves: 129 * 129S2/SvPas * C57BL/6J	MGI:7484084
cx93	Ptprz1^tm1Schl/Ptprz1^tm1Schl Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129 * 129S2/SvPas * C57BL/6J	MGI:7484075
cx94	Kat5^tm1Jwl/Kat5^+ Tg(IghMyc)22Bri/0 Trp53^tm1Tyj/Trp53^+	involves: 129 * C57BL * C57BL/6 * SJL	MGI:3814381
cx95	Trp53^tm1Tyj/Trp53^tm1Tyj Xrcc4^tm1Fwa/Xrcc4^tm1Fwa	involves: 129P2/OlaHsd * 129S2/SvPas	MGI:2653516
cx96	Trp53^tm1Tyj/Trp53^+ Xpa^tm1Hvs/Xpa^tm1Hvs	involves: 129P2/OlaHsd * 129S2/SvPas	MGI:4947935
cx97	Brca1^tm1Mak/Brca1^tm1Mak Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas	MGI:4420438
cx98	Rr149356^tm1Che/Rr149356^tm1Che Tcrd^tm1Mom/Tcrd^tm1Mom Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6	MGI:3620761
cx99	Igh^tm2Cgn/Igh^tm2Cgn Igk^tm1Rsky/Igk^tm1Rsky Trp53^tm1Tyj/Trp53^tm1Tyj Xrcc4^tm1Fwa/Xrcc4^tm1Fwa	involves: 129P2/OlaHsd * 129S2/SvPas * 129S6/SvEvTac	MGI:4437907
cx100	Igh^tm2Cgn/Igh^tm2Cgn Igk^tm1Rsky/Igk^tm1Rsky Lig4^tm1Fwa/Lig4^tm1Fwa Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas * 129S6/SvEvTac	MGI:4437910
cx101	Brca2^tm1Kamc/Brca2^tm1Kamc Trp53^tm1Tyj/Trp53^+	involves: 129P2/OlaHsd * 129S2/SvPas * BALB/c * C57BL/6	MGI:3818475
cx102	Igh^tm2.1(Tag)Rwhe/Igh^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:3850823
cx103	Nf1^tm1Tyj/Nf1^+ Suz12^Gt(Betageo)1Khe/Suz12^+ Trp53^tm1Tyj/Trp53^+	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:5699874
cx104	Cpt1c^Gt(XL823)Byg/Cpt1c^+ Nf1^tm1Tyj/Nf1^+ Trp53^tm1Tyj/Trp53^+	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:5790202
cx105	Igh^tm1.1(Tag)Rwhe/Igh^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:3850824
cx106	Sufu^Gt(XB699)Byg/Sufu^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:3759457
cx107	Trp53^tm1Tyj/Trp53^tm1Tyj Vrk1^Gt(RRR178)Byg/Vrk1^Gt(RRR178)Byg	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:6865653
cx108	Rev3l^tm1Ndew/Rev3l^tm1Ndew Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:3840908
cx109	Lyar^Gt(RRG292)Byg/Lyar^Gt(RRG292)Byg Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:6191737
cx110	Lyar^Gt(RRG292)Byg/Lyar^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:6191738
cx111	Trp53^tm1Tyj/? Zfp148^Gt(XB878)Byg/Zfp148^Gt(XB878)Byg	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:5496437
cx112	Cd44^tm1Mak/Cd44^tm1Mak Trp53^tm1Tyj/Trp53^+	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * C57BL/6J	MGI:4943188
cx113	Clp1^tm1.1Pngr/Clp1^tm1.1Pngr Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * C57BL/6J	MGI:5554932
cx114	Cul9^tm1.2Yxi/Cul9^tm1.2Yxi Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * FVB/N	MGI:5007743
cx115	Cep63^Gt(EUCE0251h11)Hmgu/Cep63^Gt(EUCE0251h11)Hmgu Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6J	MGI:5819195
cx116	Herc2^Gt(AR0530)Wtsi/Herc2^Gt(AR0530)Wtsi Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * C57BL/6	MGI:6286197
cx117	Sugt1^Gt(RRS405)Byg/Sugt1^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129P2/OlaHsd * C57BL/6J	MGI:5696984
cx118	Trp53^tm1Tyj/Trp53^tm1Tyj Tsg101^tm1Mak/Tsg101^tm1Mak	involves: 129P3/J * 129S2/SvPas * C57BL/6 * CD-1	MGI:2450866
cx119	Emg1^tm1Hdin/Emg1^tm1Hdin Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S * 129S2/SvPas * 129X1/SvJ * CD-1 * ICR	MGI:4839757
cx120	Rasal2^Gt(463C12)Cmhd/Rasal2^Gt(463C12)Cmhd Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S * 129X1/SvJ * C57BL/6 * C57BL/6NCrl	MGI:5554381
cx121	Rasal2^Gt(463C12)Cmhd/Rasal2^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S * 129X1/SvJ * C57BL/6 * C57BL/6NCrl	MGI:5554383
cx122	Bard1^tm1Thl/Bard1^tm1Thl Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S1/Sv * 129S2/SvPas	MGI:2675374
cx123	Rtel1^tm2.1Hdin/Rtel1^tm2.1Hdin Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6	MGI:5559534
cx124	Kat5^tm1Jwl/Kat5^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6	MGI:3814378
cx125	Ptch1^tm1Mps/Ptch1^+ Ptch2^tm1Pmc/Ptch2^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6	MGI:3690370
cx126	Ptch2^tm1Pmc/Ptch2^tm1Pmc Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S1/Sv * 129S2/SvPas * C57BL/6	MGI:3690369
cx127	Trp53^tm1Tyj/Trp53^+ Xrcc2^tm1Pmc/Xrcc2^tm1Pmc	involves: 129S1/Sv * 129S2/SvPas * C57BL/6	MGI:3655347
cx128	Cdkn2c^tm1Bbd/Cdkn2c^tm1Bbd Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S1/Sv * 129S2/SvPas * C57BL/6	MGI:3710321
cx129	Cdkn2c^tm1Bbd/Cdkn2c^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S1/Sv * 129S2/SvPas * C57BL/6	MGI:3710320
cx130	Cdkn2c^tm1Bbd/Cdkn2c^+ Trp53^tm1Tyj/Trp53^+	involves: 129S1/Sv * 129S2/SvPas * C57BL/6	MGI:3710319
cx131	Trp53^tm1Tyj/Trp53^tm1Tyj Xrcc2^tm1Pmc/Xrcc2^tm1Pmc	involves: 129S1/Sv * 129S2/SvPas * C57BL/6	MGI:3655298
cx132	Prmt6^tm1.2Rchd/Prmt6^tm1.2Rchd Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J * FVB/N	MGI:5509171
cx133	Terf1^tm1Tdl/Terf1^tm1Tdl Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas	MGI:2677843
cx134	Nf1^tm1Tyj/Nf1^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas	MGI:3776067
cx135	Ccnd3^tm1Pisc/Ccnd3^tm1Pisc Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas	MGI:3819978
cx136	Mdm4^tm1Glo/Mdm4^tm1Glo Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas	MGI:3850680
cx137	Mdm4^tm1Glo/Mdm4^tm1Glo Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas	MGI:3850686
cx138	Atr^tm1Ofc/Atr^tm1Ofc Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas	MGI:4355022
cx139	Rb1^tm1Tyj/Rb1^tm1Tyj Tg(Rb1)1Blg/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas	MGI:4420470
cx140	Nbn^em3Jpt/Nbn^em3Jpt Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas	MGI:6780002
cx141	Nbn^em4Jpt/Nbn^em4Jpt Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas	MGI:6780003
cx142	Gnl3^Gt(W223E05)Wrst/Gnl3^Gt(W223E05)Wrst Trp53^tm1Tyj/Trp53^tm5Tyj	involves: 129S2/SvPas * 129S4/SvJae	MGI:3702081
cx143	Trp53^tm1Tyj/Trp53^+ Trp63^tm1Fmc/Trp63^+	involves: 129S2/SvPas * 129S4/SvJae * C57BL/6	MGI:5289961
cx144	Rr149356^tm1Che/Rr149356^tm1Che Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S4/SvJae * C57BL/6	MGI:3620760
cx145	Trp53^tm1Tyj/Trp53^+ Trp73^tm1Fmc/Trp73^+	involves: 129S2/SvPas * 129S4/SvJae * C57BL/6	MGI:5289964
cx146	Nf1^tm1Tyj/? Trp53^tm1Tyj/? Mastr^129S4/SvJae/?	involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J	MGI:3587059
cx147	Nf1^tm1Tyj/? Trp53^tm1Tyj/? Mastr^C57BL/6J/?	involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J	MGI:3587060
cx148	Rad51b^tm1Kmic/Rad51b^tm1Kmic Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J	MGI:3623223
cx149	Map9^tm1.2Bcgen/Map9^tm1.2Bcgen Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S4/SvJaeSor * BALB/cJ * C57BL/6	MGI:6502662
cx150	Mdm4^tm2.1Glo/Mdm4^tm2.1Glo Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6J	MGI:3616708
cx151	Mdm4^Gt(VICTR20)7Lex/Mdm4^Gt(VICTR20)7Lex Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S5/SvEvBrd	MGI:3700235
cx152	Pip4k2b^Gt(Betageo)1Lca/Pip4k2b^Gt(Betageo)1Lca Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S5/SvEvBrd	MGI:5568932
cx153	Mdm4^Gt(VICTR20)7Lex/Mdm4^Gt(VICTR20)7Lex Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S5/SvEvBrd	MGI:3700236
cx154	Npm1^Gt(VICTR37)704Lex/Npm1^Gt(VICTR37)704Lex Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S5/SvEvBrd * C57BL/6	MGI:3608498
cx155	Rag1^tm1Fwa/Rag1^tm1Fwa Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S6/SvEvTac	MGI:5002826
cx156	Set^tm1.1Wgu/Set^tm1.1Wgu Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S6/SvEvTac	MGI:6357935
cx157	Rag1^tm1Jsek/Rag1^tm1Jsek Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S6/SvEvTac	MGI:3840834
cx158	Rag2^tm1.1Mss/Rag2^tm1.1Mss Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S6/SvEvTac	MGI:5002824
cx159	Rad50^tm2Jpt/Rad50^tm2Jpt Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6	MGI:2450431
cx160	Mdm2^tm1Glo/Mdm2^+ Mdm4^tm1Glo/Mdm4^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6	MGI:3850704
cx161	Mdm2^tm1Glo/Mdm2^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6	MGI:3850702
cx162	Bhlha15^tm2(Kras)Skz/Bhlha15^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6	MGI:3618360
cx163	Arhgap1^tm1Yizh/Arhgap1^tm1Yizh Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6	MGI:3762617
cx164	Mdm4^tm1Glo/Mdm4^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6	MGI:3850700
cx165	Hus1^tm1Led/Hus1^tm2Rsw Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6	MGI:3702291
cx166	Metap2^tm1.2Ccr/Metap2^tm1.2Ccr Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * FVB/N	MGI:3663892
cx167	Trp53^tm1Tyj/Trp53^+ Trp53bp2^tm1Xlu/Trp53bp2^tm1Xlu	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J	MGI:3629206
cx168	Trp53^tm1Tyj/Trp53^tm1Tyj Trp53bp2^tm1Xlu/Trp53bp2^tm1Xlu	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J	MGI:3629205
cx169	Trp53^tm1Tyj/Trp53^+ Trp53bp2^tm1Xlu/Trp53bp2^+	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J	MGI:3629207
cx170	Rpl27a^Sfa/Rpl27a^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J	MGI:5140356
cx171	Mdm2^tm1Glo/Mdm2^tm1Glo Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd	MGI:3850689
cx172	Dclre1a^tm1Rleg/Dclre1a^tm1Rleg Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd	MGI:4941811
cx173	Dclre1a^tm1Rleg/Dclre1a^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd	MGI:4941812
cx174	Nbn^tm1Jpt/Nbn^tm1Jpt Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd	MGI:3615887
cx175	Mdm2^tm1Glo/Mdm2^tm1Glo Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S7/SvEvBrd	MGI:3850688
cx176	Pot1a^tm1Schg/Pot1a^tm1.1Schg Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6	MGI:3690106
cx177	Mdm2^tm1Bay/Mdm2^tm1Mep Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6	MGI:3715447
cx178	Mdm2^tm1Ypz/Mdm2^tm1Ypz Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6 * FVB/N	MGI:3763436
cx179	Mdm2^tm1Ypz/Mdm2^tm1Ypz Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6 * FVB/N	MGI:3763437
cx180	Kat2a^tm1Roth/Kat2a^tm1Roth Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J	MGI:3712154
cx181	Stk11^tm1.1Mlfr/Stk11^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J	MGI:3616344
cx182	Mtbp^tm1Glo/Mtbp^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J	MGI:3803628
cx183	Mdm2^tm1Glo/Mdm2^tm1Glo Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J	MGI:2183201
cx184	Mtbp^tm1Glo/Mtbp^tm1Glo Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J	MGI:3803625
cx185	Mtbp^tm1Glo/Mtbp^tm1Glo Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J	MGI:3803626
cx186	Stk11^tm1.1Mlfr/Stk11^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J	MGI:3616343
cx187	Trp53^tm1Tyj/Trp53^tm1Tyj Xrcc1^tm1Rpe/Xrcc1^tm1Rpe	involves: 129S2/SvPas * 129X1/SvJ	MGI:2653518
cx188	Grid2^Lc-J/Grid2^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129X1/SvJ * BALB/cByJ * C57BL/6	MGI:4360675
cx189	Klf15^tm1Jain/Klf15^tm1Jain Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129X1/SvJ * C57BL/6	MGI:4888123
cx190	Ubr5^tm1Ckww/Ubr5^tm1Ckww Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129X1/SvJ * C57BL/6	MGI:3606184
cx191	Cdkn2a^tm1Cjs/Cdkn2a^tm1Cjs Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129X1/SvJ * C57BL/6	MGI:3694644
cx192	Rag2^tm2.1Desi/Rag2^tm2.1Desi Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129X1/SvJ * C57BL/6	MGI:4941323
cx193	Rag2^tm1.1Desi/Rag2^tm1.1Desi Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129X1/SvJ * C57BL/6	MGI:4941322
cx194	Dmbt1^tm1Kumc/Dmbt1^tm1Kumc Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * 129X1/SvJ * C57BL/6J	MGI:3777615
cx195	Dmbt1^tm1Kumc/Dmbt1^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * 129X1/SvJ * C57BL/6J	MGI:3777616
cx196	Nf1^tm1Tyj/? Nstr1^A/J/? Trp53^tm1Tyj/?	involves: 129S2/SvPas * A/J * C57BL/6J	MGI:3663690
cx197	Nf1^tm1Tyj/? Nstr1^C57BL/6J/Nstr1^C57BL/6J Trp53^tm1Tyj/?	involves: 129S2/SvPas * A/J * C57BL/6J	MGI:3663691
cx198	Nf1^tm1Tyj/? Nstr2^A/J/? Trp53^tm1Tyj/?	involves: 129S2/SvPas * A/J * C57BL/6J	MGI:3663692
cx199	Trp53^tm1Tyj/Trp53^tm1Tyj Wrn^tm1Lgu/Wrn^tm1Lgu	involves: 129S2/SvPas * BALB/c	MGI:3700821
cx200	Rps7^Zma/Rps7^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * BALB/c * C3H/HeH * C57BL/6J	MGI:5500165
cx201	Tg(Ela1-Tgfa)150Bri/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * BALB/c * C57BL/6 * SJL	MGI:6192108
cx202	Tg(Ela1-Tgfa)150Bri/0 Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * BALB/c * C57BL/6 * SJL	MGI:6192107
cx203	Trp53^tm1Tyj/Trp53^tm1Tyj Uimc1^tm1.2Amj/Uimc1^tm1.2Amj	involves: 129S2/SvPas * BALB/cJ * C57BL/6	MGI:5463922
cx204	Trp53^tm1Tyj/Trp53^+ Uimc1^tm1.2Amj/Uimc1^tm1.2Amj	involves: 129S2/SvPas * BALB/cJ * C57BL/6	MGI:5463923
cx205	Suprmam1^BALB/cMed/Suprmam1^BALB/cMed Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * BALB/cMed * C57BL/6 * C57BL/6J	MGI:3715519
cx206	Tg(K6ODCtr)55Tgo/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C3H * C57BL/6	MGI:3799500
cx207	Rps20^Mhdadsk4/Rps20^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C3HeB/FeJ	MGI:6260021
cx208	Rps19^Mhdadsk3/Rps19^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C3HeB/FeJ	MGI:6260014
cx209	Pclaf^tm1.1Lkd/Pclaf^tm1.1Lkd Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6	MGI:5302543
cx210	Pknox1^tm1Fbla/Pknox1^tm1Fbla Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:4839564
cx211	Thbs1^tm1Hyn/Thbs1^tm1Hyn Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6	MGI:3032768
cx212	Fdxr^tm1Xch/Fdxr^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6	MGI:6715104
cx213	Kras^tm2Tyj/Kras^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6	MGI:3770520
cx214	Fdxr^tm1Xch/Fdxr^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:6715105
cx215	Nhej1^tm1.1Ics/Nhej1^tm1.1Ics Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:5475167
cx216	Kras^tm2Tyj/Kras^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:3770519
cx217	Fos^tm1Wag/Fos^tm1Wag Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:3700989
cx218	Exo1^tm2Wed/Exo1^tm2Wed Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:5523485
cx219	Exo1^tm3.1Wed/Exo1^tm3.1Wed Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:5523487
cx220	Fos^tm1Wag/Fos^tm1Wag Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6	MGI:3700990
cx221	Thbs1^tm1Hyn/Thbs1^tm1Hyn Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:3032769
cx222	Tfdp1^tm1Lili/Tfdp1^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:2653312
cx223	Nf1^tm1Tyj/Nf1^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6	MGI:5699872
cx224	Tfdp1^tm1Lili/Tfdp1^tm1Lili Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:2653311
cx225	Prdm2^tm1Shg/Prdm2^tm1Shg Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6	MGI:3041266
cx226	Trp53^tm1Tyj/Trp53^+ Utp25^em1Glo/Utp25^em1Glo	involves: 129S2/SvPas * C57BL/6	MGI:6358197
cx227	Trp53^tm1Tyj/Trp53^tm1Tyj Utp25^em1Glo/Utp25^em1Glo	involves: 129S2/SvPas * C57BL/6	MGI:6358195
cx228	Rb1^tm1Tyj/Rb1^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6	MGI:3582787
cx229	Mdm4^tm1Zmy/Mdm4^tm1Zmy Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:5141752
cx230	Trp53^tm1Tyj/Trp53^tm1Tyj Tg(CAG-EGFP/Map1lc3b)53Nmz/0	involves: 129S2/SvPas * C57BL/6 * C57BL/6NCrj	MGI:5319199
cx231	Cenpj^tm1d(EUCOMM)Wtsi/Cenpj^tm1d(EUCOMM)Wtsi Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * C57BL/6N * FVB/NJ	MGI:5609812
cx232	Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Ly6e-MALT1)#Isg/0	involves: 129S2/SvPas * C57BL/6 * CBA	MGI:5432018
cx233	Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Prrx1-FUS/DDIT3)1Mete/0	involves: 129S2/SvPas * C57BL/6 * CBA	MGI:5430234
cx234	Tg(Trp53)1Srn/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * CBA	MGI:5751688
cx235	Tg(Pbsn-TAg)15Tvd/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * DBA/2	MGI:4836242
cx236	Suds3^tm1.1Rdp/Suds3^+ Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6 * FVB	MGI:3698864
cx237	Sin3a^tm1.1Rdp/Sin3a^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * FVB	MGI:3698865
cx238	Suds3^tm1.1Rdp/Suds3^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * FVB	MGI:3698863
cx239	Pum1^tm1.2Hfl/Pum1^tm1.2Hfl Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * FVB	MGI:5316383
cx240	Rbm38^tm1.1Xch/Rbm38^tm1.1Xch Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * FVB/N	MGI:5688514
cx241	Rbm38^tm1.1Xch/Rbm38^tm1.1Xch Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6 * FVB/N	MGI:5688515
cx242	Rbm24^tm1.1Xch/Rbm24^tm1.1Xch Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * FVB/N	MGI:6152435
cx243	Tg(Scgb1a1-rtTA)1Jaw/0 Tg(tetO-Kras2)12Hev/0 Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6 * FVB/N	MGI:5912344
cx244	Rbm24^tm1.1Xch/Rbm24^tm1.1Xch Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6 * FVB/N	MGI:6152436
cx245	Nabp2^tm1.2Nfel/Nabp2^tm1.2Nfel Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6 * FVB/N * SJL	MGI:5448647
cx246	Prkdc^scid/Prkdc^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6J	MGI:2665138
cx247	Trp53^tm1Tyj/Trp53^tm1Tyj Xrcc3^em4Mjn/Xrcc3^em4Mjn	involves: 129S2/SvPas * C57BL/6J	MGI:7310098
cx248	Trp53^tm1Tyj/Trp53^+ Xrcc3^em4Mjn/Xrcc3^em4Mjn	involves: 129S2/SvPas * C57BL/6J	MGI:7310097
cx249	Ino80^tm1.1Schg/Ino80^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6J	MGI:5898013
cx250	Rpl27a^Sfa/Rpl27a^Sfa Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6J	MGI:5140355
cx251	Prkdc^scid/Prkdc^scid Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6J	MGI:4456092
cx252	Rpl27a^Sfa/Rpl27a^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6J	MGI:5140354
cx253	Ino80^tm1.1Schg/Ino80^tm1.1Schg Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6J	MGI:5898012
cx254	Ercc6l^tm1.2Ajlc/Ercc6l^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6J * C57BL/6N * SJL/J	MGI:6283345
cx255	Ercc6l^tm1.2Ajlc/Y Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6J * C57BL/6N * SJL/J	MGI:6283343
cx256	Ercc6l^tm1.2Ajlc/Y Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6J * C57BL/6N * SJL/J	MGI:6283344
cx257	Aktip^tm1a(EUCOMM)Hmgu/Aktip^tm1a(EUCOMM)Hmgu Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6N	MGI:6315473
cx258	Rps27l^Gt(IST11658B7)Tigm/Rps27l^Gt(IST11658B7)Tigm Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6N	MGI:5707901
cx259	Rps27l^Gt(IST11658B7)Tigm/Rps27l^Gt(IST11658B7)Tigm Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6N	MGI:5707900
cx260	Aktip^tm1a(EUCOMM)Hmgu/Aktip^tm1a(EUCOMM)Hmgu Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL/6N	MGI:6315472
cx261	Trp53^tm1Tyj/Trp53^+ Tg(Ins2-Mirc13)E4Biat/0	involves: 129S2/SvPas * C57BL/6N	MGI:6829612
cx262	Trp53^tm1Tyj/Trp53^+ Zfp871^tm1a(EUCOMM)Wtsi/Zfp871^tm1a(EUCOMM)Wtsi	involves: 129S2/SvPas * C57BL/6N	MGI:7517192
cx263	Trp53^tm1Tyj/Trp53^tm1Tyj Commd10^Tg(Vav1-icre)A2Kio/Commd10^+	involves: 129S2/SvPas * C57BL/6N * C57BL/10 * CBA/Ca	MGI:6712735
cx264	Pax3^Sp/Pax3^Sp Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL * C57BL/6J * FVB	MGI:3690112
cx265	Pax3^Sp/Pax3^Sp Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * C57BL * C57BL/6J * FVB	MGI:3690111
cx266	Tg(TRP53)4Dgj/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * FVB	MGI:4819639
cx267	Tg(TRP53*R72P)7Dgj/0 Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * FVB	MGI:4819640
cx268	Tg(MMTV-AURKA)#Cxd/? Trp53^tm1Tyj/Trp53^+	involves: 129S2/SvPas * FVB/N	MGI:3836158
cx269	Pip4k2a^tm1.2Lca/Pip4k2a^tm1.2Lca Pip4k2b^Gt(Betageo)1Lca/Pip4k2b^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S/SvEv * 129S2/SvPas * 129S5/SvEvBrd	MGI:5568940
cx270	Ssbp2^tm1Lana/Ssbp2^tm1Lana Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S/SvEv * 129S2/SvPas * BALB/c * C57BL/6	MGI:4462851
cx271	Brca2^tm1Arge/Brca2^tm1Arge Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S/SvEv * 129S2/SvPas * C57BL/6	MGI:2177218
cx272	Nf1^tm1Fcr/Nf1^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S/SvEv * 129S2/SvPas * C57BL/6	MGI:3580070
cx273	Nf1^tm1Fcr/Nf1^+ Trp53^tm1Tyj/Trp53^+	involves: 129S/SvEv * 129S2/SvPas * C57BL/6	MGI:3580069
cx274	Brca1^tm1Arge/Brca1^tm1Arge Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S/SvEv * 129S2/SvPas * C57BL/6	MGI:2177217
cx275	Rag2^tm1Fwa/Rag2^tm1Fwa Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S/SvEv * 129S2/SvPas * C57BL/6J	MGI:2665118
cx276	Rag2^tm1Fwa/Rag2^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S/SvEv * 129S2/SvPas * C57BL/6J	MGI:2665119
cx277	Cdkn2a^tm1.1Brn/Cdkn2a^tm1.1Brn Pknox1^tm1Fbla/Pknox1^tm1Fbla Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129/Sv * 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:4839565
cx278	Tg(IghMyc)22Bri/0 Trp53^tm1Tyj/Trp53^+	involves: 129/Sv * 129X1/SvJ * C57BL * C57BL/6 * SJL	MGI:3814379
cx279	Dph1^tm2Bhr/Dph1^+ Trp53^tm1Tyj/Trp53^+	involves: 129/Sv * C57BL/6	MGI:3033461
cx280	Dph1^tm2Bhr/Dph1^tm2Bhr Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129/Sv * C57BL/6	MGI:3033460
cx281	Nf1^tm1Tyj/Nf1^+ Trp53^tm1Tyj/Trp53^+	involves: 129/Sv * C57BL/6	MGI:3580073
cx282	Motp1^CE/J/Motp1^CE/J Trp53^tm1Tyj/Trp53^+	involves: 129-Trp53^tm1Tyj/J * CE/J	MGI:3575575
cx283	Motp1^CE/J/Motp1^CE/J Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129-Trp53^tm1Tyj/J * CE/J	MGI:3575574
cx284	Susd6^tm1.1Geno/Susd6^tm1.1Geno Trp53^tm1Tyj/Trp53^tm1Tyj	involves: C57BL/6J	MGI:5606045
cx285	Susd6^tm1.1Geno/Susd6^+ Trp53^tm1Tyj/Trp53^tm1Tyj	involves: C57BL/6J	MGI:5606044
cx286	Nf1^tm1Tyj/Nf1^+ Trp53^tm1Tyj/Trp53^+	(SJL/J x B6.129S2-Trp53^tm1Tyj Nf1^tm1Tyj/+ +)F1	MGI:5286082

Genotype
MGI:3769499

hm1

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: 129S6.129-Trp53^tm1Tyj Rb1^tm1.1Jyjw

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

mortality/aging

premature death ( J:102483 )

• mice become moribund from lymphoma involving various tissues within >30 weeks; mice with aggressive lymphoma have a mean survival time of 18 weeks

neoplasm

increased lymphoma incidence ( J:102483 )

• mice develop lymphomas

increased teratoma incidence ( J:102483 )

• median survival time of mice with teratomas is 7 weeks

• no mice living beyond median survival age show extratesticular teratomas

increased testicular teratoma incidence ( J:102483 )

♂

digestive/alimentary system

intestinal ulcer ( J:102483 )

• after 7 days of dextran sodium sulfate treatment, mice develop large ulcers in the colon

growth/size/body

weight loss ( J:102483 )

• with DSS treatment, double mutants have an average weight of 14% of body weight

reproductive system

increased testicular teratoma incidence ( J:102483 )

♂

endocrine/exocrine glands

increased testicular teratoma incidence ( J:102483 )

♂

Genotype
MGI:3849871

hm2

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: 129-Trp53^tm1Tyj/J

cardiovascular system

abnormal retina vasculature morphology ( J:55873 )

• Background Sensitivity: abnormally dilated peripheral retinal blood vessels, with some mice exhibiting thin blood vessels extending from the optic nerve head toward the lens, but few reach the lens surface

vision/eye

abnormal retina vasculature morphology ( J:55873 )

• Background Sensitivity: abnormally dilated peripheral retinal blood vessels, with some mice exhibiting thin blood vessels extending from the optic nerve head toward the lens, but few reach the lens surface

Genotype
MGI:3849876

hm3

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: B6.129S2-Trp53^tm1Tyj/J

cardiovascular system

abnormal retina vasculature morphology ( J:55873 )

• Background Sensitivity: abnormal blood vessels are found to extend from the peripapillary inner retina through the posterior vitreous and into the retrolental membranes

• abnormally dilated peripheral retinal blood vessels

vision/eye

abnormal posterior eye segment morphology ( J:55873 )

• Background Sensitivity: on the C57BL/6J background aberrant ocular phenotypes are observed as early as 14 days of age

abnormal optic nerve morphology ( J:55873 )

• Background Sensitivity: the pial septae in many areas are disorganized on the C57BL/6J background but not the 129 or F1 backgrounds

optic nerve degeneration ( J:55873 )

• Background Sensitivity: degeneration is found to varying degrees on the C57BL/6J background, but not the 129 background

optic nerve hypoplasia ( J:55873 )

• Background Sensitivity: bilateral or unilateral optic nerve hypoplasia is found on the C57BL/6J background, but not on the 129 or F1 background

abnormal ocular fundus morphology ( J:55873 )

• Background Sensitivity: pigmented or nonpigmented fibrous retrolental tissue is commonly found in homozygotes on the C57BL/6J background

abnormal retina vasculature morphology ( J:55873 )

• Background Sensitivity: abnormal blood vessels are found to extend from the peripapillary inner retina through the posterior vitreous and into the retrolental membranes

• abnormally dilated peripheral retinal blood vessels

retina fold ( J:55873 )

• Background Sensitivity: retinal folds are found in some homozygotes on the C57BL/6J background

increased opacity of vitreous body ( J:55873 )

• Background Sensitivity: fine snowflake-like vitreal opacities can be found on the C57BL/6J background by 21 days of age and may result from the accumulation of fibrous and vascular debris in the vitreous

nervous system

abnormal optic nerve morphology ( J:55873 )

• Background Sensitivity: the pial septae in many areas are disorganized on the C57BL/6J background but not the 129 or F1 backgrounds

optic nerve degeneration ( J:55873 )

• Background Sensitivity: degeneration is found to varying degrees on the C57BL/6J background, but not the 129 background

optic nerve hypoplasia ( J:55873 )

• Background Sensitivity: bilateral or unilateral optic nerve hypoplasia is found on the C57BL/6J background, but not on the 129 or F1 background

Genotype
MGI:7484074

hm4

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129 * 129S2/SvPas * C57BL/6J

neoplasm

neoplasm ( J:243104 )

N • contact Xray and histological analysis of undecalcified spine or tibia sections revealed no signs of osteosarcoma development at 12 weeks of age

Genotype
MGI:3584474

hm5

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas

mortality/aging

premature death ( J:88120 , J:95316 )

• animals die by about 26 weeks (J:88120)

• mean life span is 4.4 months (J:95316)

decreased tumor-free survival time ( J:132597 )

• majority of mice (82%) die before 9 months of age, or are euthanized due to occurrence of obvious tumor mass

prenatal lethality, incomplete penetrance ( J:95316 )

• a slight decrease is seen in the number of females born

growth/size/body

cardiac hypertrophy ( J:120332 )

• increased hypertrophy as a result of transverse aortic restriction

nervous system

abnormal neuron differentiation ( J:102702 )

• GNPs from mutants show ~50% levels of proliferation compared to Cdkn2c, Trp53-double null cells after 3 days in culture and levels of cells incorporating BrdU are still less in single mutants in tests where cells are stimulated with Shh after culture

increased medulloblastoma incidence ( J:102702 )

• 13/19 (68%) of animals receiving 4 Gy radiation at P5 or 6 develop cerebellar tumors

neoplasm

increased tumor incidence ( J:95316 )

• 32% have multiple tumors

increased lymphoma incidence ( J:221224 )

• 3 of 10 mice develop lymphomas involving the spleen and lymph nodes

increased T cell derived lymphoma incidence ( J:88120 , J:95316 , J:221224 , J:251434 )

• mice start to develop T cell malignancies at 14-16 weeks (J:88120)

• 66% of homozygotes display hematological malignancies, primarily T cell lymphomas (J:95316)

• 6 of 10 mice develop thymic lymphomas (J:221224)

• mice present with thymic lymphoma at around 180 days of age (J:251434)

increased medulloblastoma incidence ( J:102702 )

• 13/19 (68%) of animals receiving 4 Gy radiation at P5 or 6 develop cerebellar tumors

increased hemangiosarcoma incidence ( J:95316 )

• the incidence of hemangiosarcomas is 32% compared to 62% in Trp53^tm1Tyj/Trp53^tm2.1Tyj mice

cellular

polyploidy ( J:109354 )

• after irradiation with UVC light, MEFs from null mice show higher levels of polyploidy than Trp53^tm2Xu homozygotes

abnormal cell cycle checkpoint function ( J:77907 , J:126920 )

• gamma-irradiation fails to produce an increase in the relative number of cells in G1 compared to S phase (J:77907)

• mouse embryonic fibroblasts exposed to radiation fail to arrest at the G1/S transition unlike similarly treated wild-type cells (J:126920)

decreased cellular sensitivity to ultraviolet irradiation ( J:77907 )

• reduced sensitivity to UV-induced cell death in MEFs compared to wild-type cells

decreased T cell apoptosis ( J:109354 )

• thymocytes are essentially resistant to Trp53-mediated apoptosis

decreased thymocyte apoptosis ( J:126920 , J:158953 , J:195018 )

• rare following exposure to ionizing radiation (J:126920)

• in response to irradiation (J:158953)

• in irradiated thymocytes (J:195018)

decreased splenocyte apoptosis ( J:195018 )

• in irradiated spleen cells

abnormal neuron differentiation ( J:102702 )

• GNPs from mutants show ~50% levels of proliferation compared to Cdkn2c, Trp53-double null cells after 3 days in culture and levels of cells incorporating BrdU are still less in single mutants in tests where cells are stimulated with Shh after culture

increased fibroblast proliferation ( J:77907 )

• in MEFs

immune system

decreased T cell apoptosis ( J:109354 )

• thymocytes are essentially resistant to Trp53-mediated apoptosis

decreased thymocyte apoptosis ( J:126920 , J:158953 , J:195018 )

• rare following exposure to ionizing radiation (J:126920)

• in response to irradiation (J:158953)

• in irradiated thymocytes (J:195018)

decreased splenocyte apoptosis ( J:195018 )

• in irradiated spleen cells

cardiovascular system

increased angiogenesis ( J:120332 )

• increased number of microvessels form 2 weeks after transverse aortic constriction

cardiac hypertrophy ( J:120332 )

• increased hypertrophy as a result of transverse aortic restriction

abnormal cardiovascular system physiology ( J:120332 )

• better systolic function than control

hematopoietic system

decreased T cell apoptosis ( J:109354 )

• thymocytes are essentially resistant to Trp53-mediated apoptosis

decreased thymocyte apoptosis ( J:126920 , J:158953 , J:195018 )

• rare following exposure to ionizing radiation (J:126920)

• in response to irradiation (J:158953)

• in irradiated thymocytes (J:195018)

decreased splenocyte apoptosis ( J:195018 )

• in irradiated spleen cells

endocrine/exocrine glands

decreased thymocyte apoptosis ( J:126920 , J:158953 , J:195018 )

• rare following exposure to ionizing radiation (J:126920)

• in response to irradiation (J:158953)

• in irradiated thymocytes (J:195018)

increased T cell derived lymphoma incidence ( J:88120 , J:95316 , J:221224 , J:251434 )

• mice start to develop T cell malignancies at 14-16 weeks (J:88120)

• 66% of homozygotes display hematological malignancies, primarily T cell lymphomas (J:95316)

• 6 of 10 mice develop thymic lymphomas (J:221224)

• mice present with thymic lymphoma at around 180 days of age (J:251434)

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Li-Fraumeni syndrome		DOID:3012	OMIM:PS151623	J:95316

Genotype
MGI:3616345

hm6

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J

neoplasm

decreased tumor incidence ( J:104347 )

• median age of survival is 17 months compared to 11 months in mice heterozygous for Stk11^tm1.1Mlfr and Trp53^tm1Tyj

Genotype
MGI:3695127

hm7

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * BALB/c

cellular

increased cellular sensitivity to ionizing radiation ( J:116176 )

• at P10, pattern and extent of oocyte loss in ovaries of mutants after exposure to 0.45 Gy radiation on P5 is similar to wild-type and much more sever than Trp63^tm2Fmc mutants

Genotype
MGI:2174782

hm8

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:72391 , J:95318 )

• average life span 160 days (J:72391)

• homozygous mutants die between ~50 to 250 days after birth (J:95318)

decreased tumor-free survival time ( J:87501 )

• 90% succumb to tumors and die by 7 months of age

preweaning lethality, incomplete penetrance ( J:17728 )

• 16.6% rather than the expected 25% of mutants are observed at weaning, indicating partial lethality either during embryogenesis or after birth but before weaning

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:17728 , J:87501 )

• most lymphomas are thymic lymphomas (J:17728)

• 75% of observed tumors are thymic lymphomas (J:87501)

homeostasis/metabolism

abnormal iron homeostasis ( J:244082 )

• mouse embryonic fibroblasts (MEFs) show increased protein expression of IREB2 (iron responsive element binding protein 2; aka IRP2) and TFRC (transferrin receptor; aka TfR1) but reduced expression of ACO1 (aconitase 1; aka IRP1) and FTH1 (ferritin heavy polypeptide 1)

abnormal iron level ( J:244082 )

• Pearl's Prussian blue staining revealed mild iron overload in E8.0 embryos

• MEFs show mitochondrial iron accumulation

abnormal protein level ( J:244082 )

• MEFs show reduced protein levels of FDXR and CDKN1A (aka p21)

neoplasm

increased tumor incidence ( J:17728 , J:72391 )

• predominantly lymphomas with sarcomas and teratomas (J:17728)

increased hemangioma incidence ( J:72391 )

• 3.3% incidence

increased lymphoma incidence ( J:17728 , J:72391 , J:95318 )

• 71% of mice develop lymphoma, usually affecting the thymus (J:17728)

• 70% incidence (J:72391)

• 56% of homozygous nulls developed lymphomas (J:95318)

increased T cell derived lymphoma incidence ( J:17728 , J:87501 )

• most lymphomas are thymic lymphomas (J:17728)

• 75% of observed tumors are thymic lymphomas (J:87501)

increased carcinoma incidence ( J:72391 )

• 3.3% incidence

increased squamous cell carcinoma incidence ( J:72391 )

• 3.3% incidence of stomach squamous cell carcinoma

increased sarcoma incidence ( J:17728 , J:72391 , J:95318 )

• 50% incidence (J:72391)

• 40% of homozygous nulls developed sarcomas (J:95318)

increased rhabdomyosarcoma incidence ( J:17728 )

increased fibrosarcoma incidence ( J:72391 )

• 13% incidence

increased hemangiosarcoma incidence ( J:17728 , J:72391 )

• 20% incidence (J:72391)

increased osteosarcoma incidence ( J:17728 , J:72391 )

• 13% incidence (J:72391)

increased teratoma incidence ( J:17728 )

cellular

aneuploidy ( J:87501 )

abnormal mitochondrial morphology ( J:244082 )

• MEFs show mitochondrial iron accumulation

decreased cellular sensitivity to gamma-irradiation ( J:95318 )

• irradiated E13.5 heterozygous embryos showed no evidence of apoptosis in the hypothalamus compared to wildtype and heterozygotes that showed a high number of apoptotic cells

decreased cellular sensitivity to ultraviolet irradiation ( J:170976 )

• in mouse embryonic fibroblasts

abnormal apoptosis ( J:87501 )

increased fibroblast proliferation ( J:95318 )

• MEFs initially did not show any significant differences in growth rate but by day 4, grew more rapidly than wildtype or heterozygous MEFs

decreased cell proliferation ( J:170976 )

• in mouse embryonic fibroblasts treated with UV irradiation

muscle

increased rhabdomyosarcoma incidence ( J:17728 )

skeleton

increased osteosarcoma incidence ( J:17728 , J:72391 )

• 13% incidence (J:72391)

digestive/alimentary system

colon polyps ( J:72391 )

• 6.7% incidence

gastric polyps ( J:72391 )

• 3.3% incidence of stomach polyps

Genotype
MGI:5751693

hm9

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * CBA

cellular

decreased thymocyte apoptosis ( J:80311 )

• radiation-induced apoptosis in the thymus is decreased as compared to wild-type

endocrine/exocrine glands

decreased thymocyte apoptosis ( J:80311 )

• radiation-induced apoptosis in the thymus is decreased as compared to wild-type

hematopoietic system

decreased thymocyte apoptosis ( J:80311 )

• radiation-induced apoptosis in the thymus is decreased as compared to wild-type

immune system

decreased thymocyte apoptosis ( J:80311 )

• radiation-induced apoptosis in the thymus is decreased as compared to wild-type

mortality/aging

premature death ( J:80311 )

• average lifespan is 4.5 months

Genotype
MGI:5688516

hm10

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB/N

mortality/aging

decreased mortality induced by ionizing radiation ( J:216929 )

• median survival following exposure to 8 gray of whole body gamma-irradiation is 34 days

premature death ( J:216929 )

• longest lifespan is 34 weeks, median survival is 25 weeks

homeostasis/metabolism

decreased mortality induced by ionizing radiation ( J:216929 )

• median survival following exposure to 8 gray of whole body gamma-irradiation is 34 days

Genotype
MGI:4420446

hm11

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * FVB/N

cellular

decreased cellular sensitivity to ionizing radiation ( J:114161 )

• following ionizing radiation treatment, hair follicles do not exhibit apoptosis unlike in similarly treated wild-type mice

• following ionizing radiation treatment, arrested cell growth in the epidermis is partially abrogated compared to in similarly treated wild-type mice

integument

decreased sensitivity to skin irradiation ( J:114161 )

• following ionizing radiation treatment, arrested cell growth in the epidermis is partially abrogated compared to in similarly treated wild-type mice

Genotype
MGI:7484082

ht12

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129 * 129S2/SvPas * C57BL/6J

neoplasm

neoplasm ( J:243104 )

N • no mice (0 of 24) exhibit obvious skeletal tumors (osteosarcomas) at 52 weeks of age

Genotype
MGI:3818474

ht13

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * BALB/c * C57BL/6

mortality/aging

decreased survivor rate ( J:109193 )

• 50% survival at 63 weeks

Genotype
MGI:3584473

ht14

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas

renal/urinary system

increased urinary system tumor incidence ( J:170769 )

• 12 of 45 mice treated with 2-AAF develop urinary bladder tumors

mortality/aging

premature death ( J:95316 )

• mean life span is 15.4 months

neoplasm

increased tumor incidence ( J:95316 )

• 19% have multiple tumors compared to 44% of Trp53^tm3.1Tyj heterozygotes

increased incidence of tumors by chemical induction ( J:170769 )

• 12 of 45 mice treated with 2-AAF develop urinary bladder tumors

increased carcinoma incidence ( J:95316 )

• 4 of 37 develop low grade carcinomas including 1 with a well differentiated lung carcinoma

increased urinary system tumor incidence ( J:170769 )

• 12 of 45 mice treated with 2-AAF develop urinary bladder tumors

cellular

decreased cellular sensitivity to gamma-irradiation ( J:259337 )

• in thymocytes exposed to gamma radiation

decreased thymocyte apoptosis ( J:158953 )

• in response to irradiation

increased fibroblast proliferation ( J:95316 )

• a larger fraction of MEFs are in S phase compared to wild-type mice

hematopoietic system

abnormal hematopoietic system physiology ( J:158953 )

• hematopoietic stem and progenitor cells (HSPC) from irradiated mice transplanted into irradiated mice reconstitute the HSPC population exhibit a competitive advantage over HSPC from untreated mice compared with cells from similarly irradiated wild-type mice

• however, no competitive advantage is observed over similarly treated Cdkn2a^tm2.1Rdp cells in irradiation chimera experiments

decreased thymocyte apoptosis ( J:158953 )

• in response to irradiation

immune system

decreased thymocyte apoptosis ( J:158953 )

• in response to irradiation

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:170769 )

• 12 of 45 mice treated with 2-AAF develop urinary bladder tumors

endocrine/exocrine glands

decreased thymocyte apoptosis ( J:158953 )

• in response to irradiation

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Li-Fraumeni syndrome		DOID:3012	OMIM:PS151623	J:95316

Genotype
MGI:5463925

ht15

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * BALB/cJ * C57BL/6

neoplasm

abnormal tumor incidence ( J:191827 )

• 42.8% of mice (6 of 14) develop thymic lymphomas after exposure to ionizing radiation

Genotype
MGI:2174783

ht16

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:95318 )

• heterozygous mutants die between 150 to 750 days after birth

decreased tumor-free survival time ( J:17728 , J:135509 )

• 28% of mutants die by 17 months of age due to tumors (J:17728)

• less than 5% of mice live past two years due to cancerous tumors (J:135509)

neoplasm

abnormal tumor morphology ( J:17728 )

• tumors show loss of heterozygosity for Trp53

increased tumor incidence ( J:17728 , J:135509 )

• age of onset 9 months (J:17728)

• over 95% of mice have tumors by 2 years of age (J:135509)

increased pancreas tumor incidence ( J:72391 )

• 2.9% incidence of pancreatic adenocarcinomas

increased adenoma incidence ( J:72391 )

• 5.9% incidence

increased leukemia incidence ( J:135509 )

• is observed in 2.6% of mice by 24 months of age

increased lymphoma incidence ( J:17728 , J:72391 )

• 25% of mutants exhibit lymphomas (J:17728)

• 32% incidence (J:72391)

increased histiocytic sarcoma incidence ( J:72391 )

• 15% incidence

increased carcinoma incidence ( J:72391 , J:95318 )

• 35% incidence of carcinomas (J:72391)

• 2.9% incidence of pancreatic adenocarcinomas (J:72391)

• 12% of heterozygous mutants developed carcinomas, which are rare in homozygotes (J:95318)

increased adenocarcinoma incidence ( J:72391 )

• 18% incidence

increased mammary adenocarcinoma incidence ( J:72391 )

• 2.9% incidence

increased lung adenocarcinoma incidence ( J:72391 )

• 12% incidence

increased squamous cell carcinoma incidence ( J:72391 )

• 18% incidence of ear squamous cell carcinoma

increased sarcoma incidence ( J:17728 , J:72391 , J:95318 )

• 57% of mutants exhibit sarcomas (J:17728)

• 56% incidence of sarcomas (J:72391)

• 2.9% incidence of undifferentiated sarcomas (J:72391)

• 56% of heterozygous mutants developed sarcomas (J:95318)

increased leiomyosarcoma incidence ( J:17728 )

increased rhabdomyosarcoma incidence ( J:17728 )

increased fibrosarcoma incidence ( J:17728 )

increased hemangiosarcoma incidence ( J:17728 , J:72391 )

• 8.8% incidence (J:72391)

increased osteosarcoma incidence ( J:17728 , J:72391 )

• 29% incidence (J:72391)

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:72391 )

• 2.9% incidence

increased pancreas tumor incidence ( J:72391 )

• 2.9% incidence of pancreatic adenocarcinomas

integument

increased mammary adenocarcinoma incidence ( J:72391 )

• 2.9% incidence

digestive/alimentary system

intestine polyps ( J:72391 )

• 2.9% incidence of small intestinal polyps

gastric polyps ( J:72391 )

• 2.9% incidence of stomach polyps

muscle

increased leiomyosarcoma incidence ( J:17728 )

increased rhabdomyosarcoma incidence ( J:17728 )

respiratory system

increased lung adenocarcinoma incidence ( J:72391 )

• 12% incidence

skeleton

increased osteosarcoma incidence ( J:17728 , J:72391 )

• 29% incidence (J:72391)

homeostasis/metabolism

abnormal iron level ( J:244082 )

• Pearl's Prussian blue staining revealed mild iron overload in E8.0 embryos

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Li-Fraumeni syndrome		DOID:3012	OMIM:PS151623	J:17728

Genotype
MGI:5751694

ht17

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * CBA

cellular

decreased thymocyte apoptosis ( J:80311 )

• radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53^tm1Tyj mice, but is decreased as compared to wild-type

endocrine/exocrine glands

decreased thymocyte apoptosis ( J:80311 )

• radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53^tm1Tyj mice, but is decreased as compared to wild-type

hematopoietic system

decreased thymocyte apoptosis ( J:80311 )

• radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53^tm1Tyj mice, but is decreased as compared to wild-type

immune system

decreased thymocyte apoptosis ( J:80311 )

• radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53^tm1Tyj mice, but is decreased as compared to wild-type

mortality/aging

premature death ( J:80311 )

• average lifespan is 14 months

Genotype
MGI:5688517

ht18

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB/N

mortality/aging

premature death ( J:216929 )

• median survival is 64 weeks

Genotype
MGI:3629208

ht19

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

neoplasm

abnormal tumor incidence ( J:108701 )

• compound mutants which are heterozygous for Trp53^tm1Tyj and homozygous wild-type for Trp53bp2 show 7% tumor development over 72 weeks

abnormal tumor latency ( J:108701 )

• mice show a significant difference in tumor onset compared to Trp53bp2^tm1Xlu/+ Trp53^tm1Tyj homozygous mice

Genotype
MGI:3584464

ht20

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm2.1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae

mortality/aging

premature death ( J:95316 )

• mean life span is 4.5 months

prenatal lethality, incomplete penetrance ( J:95316 )

• a slight decrease is seen in the number of females born

neoplasm

increased tumor incidence ( J:95316 )

• 57% have multiple tumors, significantly more than in Trp53^tm1Tyj homozygotes (32%)

increased T cell derived lymphoma incidence ( J:95316 )

• a slight decrease in hematological malignancies (primarily T cell lymphomas) is seen compared to Trp53^tm1Tyj homozygotes (50% compared to 66%)

increased carcinoma incidence ( J:95316 )

• carcinomas are seen in 16% of mice, with most carcinomas showing signs of invasion, metastasis, or other features of advanced human carcinomas

• most carcinomas are derived from epithelial cells

increased hemangiosarcoma incidence ( J:95316 )

• the incidence of hemangiosarcomas is increased to 62% compared to 32% in Trp53^tm1Tyj homozygotes and these tumors are highly aggressive

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:95316 )

• a slight decrease in hematological malignancies (primarily T cell lymphomas) is seen compared to Trp53^tm1Tyj homozygotes (50% compared to 66%)

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Li-Fraumeni syndrome		DOID:3012	OMIM:PS151623	J:95316

Genotype
MGI:3584471

ht21

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm3.1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae

mortality/aging

premature death ( J:95316 )

• mean life span is 4.6 months

prenatal lethality, incomplete penetrance ( J:95316 )

• a slight decrease is seen in the number of females born

neoplasm

increased tumor incidence ( J:95316 )

• 43% have multiple tumors

increased T cell derived lymphoma incidence ( J:95316 )

• a slight decrease in hematological malignancies (primarily T cell lymphomas) is seen compared to Trp53^tm1Tyj homozygotes (55% compared to 66%)

increased carcinoma incidence ( J:95316 )

• carcinomas are seen in 18% of mice, with most carcinomas showing signs of invasion, metastasis, or other features of advanced human carcinomas

• most carcinomas are derived from epithelial cells

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:95316 )

• a slight decrease in hematological malignancies (primarily T cell lymphomas) is seen compared to Trp53^tm1Tyj homozygotes (55% compared to 66%)

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Li-Fraumeni syndrome		DOID:3012	OMIM:PS151623	J:95316

Genotype
MGI:5790354

ht22

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1.1Umol
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * C57BL/6NTac

mortality/aging

premature death ( J:228632 )

• shortened survival compared to single Trp53^tm1Tyj homozygotes

neoplasm

increased leukemia incidence ( J:228632 )

• T-lymphoma cell lines established from mutant mice develop into highly aggressive leukemias when tail vein injected into the circulation of nude mice

increased lymphoma incidence ( J:228632 )

• lymphomas show a 2-fold increase in cell proliferation compared to lymphomas from Trp53^tm1Tyj homozygotes and compound heterozygous Trp53^tm2.1Umol/Trp53^tm1Tyj mice

increased T cell derived lymphoma incidence ( J:228632 )

• accelerated tumor onset of T lymphomas compared to single Trp53^tm1Tyj homozygotes

increased B cell derived lymphoma incidence ( J:228632 )

• accelerated tumor onset of B lymphomas compared to single Trp53^tm1Tyj homozygotes

increased carcinoma incidence ( J:228632 )

• mice show broadening of the tumor spectrum, showing more carcinomas compared with single Trp53^tm1Tyj homozygotes

increased sarcoma incidence ( J:228632 )

• mice show broadening of the tumor spectrum, showing a higher diversity of sarcoma subtypes compared with single Trp53^tm1Tyj homozygotes

increased reproductive system tumor incidence ( J:228632 )

• mice show broadening of the tumor spectrum, showing more germ cell tumors compared with single Trp53^tm1Tyj homozygotes

decreased tumor latency ( J:228632 )

• accelerated tumor onset of T lymphomas, B lymphomas, and solid tumors compared to single Trp53^tm1Tyj homozygotes

cellular

decreased cellular sensitivity to gamma-irradiation ( J:228632 )

• thymocytes are resistant to apoptosis after gamma-irradiation

embryo

abnormal mesenchyme morphology ( J:228632 )

• mice show a similar expansion of mesenchymal stem cells as single Trp53^tm1Tyj homozygotes

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:228632 )

• accelerated tumor onset of T lymphomas compared to single Trp53^tm1Tyj homozygotes

hematopoietic system

increased hematopoietic stem cell number ( J:228632 )

• mice show a greater increase in the number of hematopoietic Lin-Sca1+c-Kit+ (LSK) progenitor cells than single Trp53^tm1Tyj homozygotes

reproductive system

increased reproductive system tumor incidence ( J:228632 )

• mice show broadening of the tumor spectrum, showing more germ cell tumors compared with single Trp53^tm1Tyj homozygotes

Genotype
MGI:5790358

ht23

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm2.1Umol
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * C57BL/6NTac

mortality/aging

premature death ( J:228632 )

• mice show similar survival to single Trp53^tm1Tyj homozygotes

• however, beyond 230 days, mice show a trend toward survival extension compared to single Trp53^tm1Tyj homozygotes, most likely due to a reduction in very late appearing B lymphomas

neoplasm

increased lymphoma incidence ( J:228632 )

• lymphomas show a decrease in cell proliferation compared to lymphomas from compound heterozygous Trp53^tm1.1Umol/Trp53^tm1Tyj mice

increased T cell derived lymphoma incidence ( J:228632 )

• mice show similar tumor latency as single Trp53^tm1Tyj homozygotes

increased B cell derived lymphoma incidence ( J:228632 )

• mice show similar tumor latency as single Trp53^tm1Tyj homozygotes

increased carcinoma incidence ( J:228632 )

• mice show broadening of the tumor spectrum, showing more carcinomas compared with single Trp53^tm1Tyj homozygotes

increased sarcoma incidence ( J:228632 )

• mice show broadening of the tumor spectrum, showing a higher diversity of sarcoma subtypes compared with single Trp53^tm1Tyj homozygotes

increased reproductive system tumor incidence ( J:228632 )

• mice show broadening of the tumor spectrum, showing more germ cell tumors compared with single Trp53^tm1Tyj homozygotes

reproductive system

increased reproductive system tumor incidence ( J:228632 )

• mice show broadening of the tumor spectrum, showing more germ cell tumors compared with single Trp53^tm1Tyj homozygotes

cellular

decreased cellular sensitivity to gamma-irradiation ( J:228632 )

• thymocytes are resistant to apoptosis after gamma-irradiation

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:228632 )

• mice show similar tumor latency as single Trp53^tm1Tyj homozygotes

hematopoietic system

increased hematopoietic stem cell number ( J:228632 )

• mice show a similar increase in the number of hematopoietic Lin-Sca1+c-Kit+ (LSK) progenitor cells as single Trp53^tm1Tyj homozygotes

Genotype
MGI:3722619

ht24

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm3.1Glo
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6

mortality/aging

premature death ( J:95318 )

• mice do not survive past 300 days compared to Trp53^tm1Tyj heterozygotes and Trp53^tm3.1Glo heterozygotes that live to 900 days

Genotype
MGI:5306614

cn25

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1.1Dgk
• Genetic Background: involves: 129S * 129X1/SvJ * C57BL/6

cellular

increased cell proliferation ( J:180576 )

• in mouse embryonic fibroblasts transfected with a flpo-expressing adenovirus

delayed cellular replicative senescence ( J:180576 )

• in mouse embryonic fibroblasts transfected with a flpo-expressing adenovirus

Genotype
MGI:3819400

cn26

• Allelic Composition: Telo2^tm1Tdl/Telo2^tm1.1Tdl; Trp53^tm1Tyj/Trp53^tm1Tyj; Gt(ROSA)26Sor^{tm1(cre/ERT)Nat}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129 * 129P2/OlaHsd * 129S2/SvPas * C57BL/6J

cellular

abnormal cell cycle ( J:141633 )

• tamoxifen-treated mouse embryonic fibroblasts exhibit cell cycle arrest after 6 days in culture unlike wild-type cells

Genotype
MGI:4443108

cn27

• Allelic Composition: Gt(ROSA)26Sor^{tm1(CAG-Trp53*,-EGFP)Medz}/Gt(ROSA)26Sor^{tm1(cre/ERT)Nat}; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129 * 129S2/SvPas * C57BL/6

hematopoietic system

hematopoietic system phenotype ( J:158953 )

N • hematopoietic stem and progenitor cells of irradiated mice treated with tamoxifen do not exhibit a selective advantage over cells not expressing the modified cDNA

Genotype
MGI:4443109

cn28

• Allelic Composition: Gt(ROSA)26Sor^{tm1(CAG-Trp53*,-EGFP)Medz}/Gt(ROSA)26Sor^{tm1(cre/ERT)Nat}; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129 * 129S2/SvPas * C57BL/6

hematopoietic system

hematopoietic system phenotype ( J:158953 )

N • hematopoietic stem and progenitor cells of irradiated mice treated with tamoxifen do not exhibit a selective advantage over cells not expressing the modified cDNA

Genotype
MGI:5523425

cn29

• Allelic Composition: Gnl3^tm2.1Rylt/Gnl3^tm2.1Rylt; Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(CAG-cre/Esr1*)5Amc/0
• Genetic Background: involves: 129 * 129S2/SvPas * C57BL/6 * CBA

cellular

abnormal cell physiology ( J:198698 )

• increase in the percentage of MEFs showing signs of replication-induced DNA damage after tamoxifen treatment

abnormal cell death ( J:198698 )

• tamoxifen treatment shortens the lifespan of MEFs

decreased fibroblast proliferation ( J:198698 )

• tamoxifen treatment impairs the long-term proliferative potential of MEFs

Genotype
MGI:4357787

cn30

• Allelic Composition: Terf1^tm1.1Blas/Terf1^tm1.1Blas; Tg(KRT5-cre)1Tak/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129 * C3H * C57BL/6 * SJL

mortality/aging

mortality/aging ( J:152077 )

N • perinatal and early postnatal lethality is normal

neoplasm

increased skin squamous cell carcinoma incidence ( J:152077 )

• in tail and ear skin of older mice

craniofacial

oral leukoplakia ( J:152077 )

digestive/alimentary system

oral leukoplakia ( J:152077 )

integument

integument phenotype ( J:152077 )

N • hair growth and skin pigmentation are normal

abnormal nail morphology ( J:152077 )

increased skin squamous cell carcinoma incidence ( J:152077 )

• in tail and ear skin of older mice

growth/size/body

oral leukoplakia ( J:152077 )

Genotype
MGI:3783542

cn31

• Allelic Composition: Cops5^tm1Rpar/Cops5^tm1Rpar; Tg(Lck-cre)548Jxm/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129 * C57BL/6 * CBA * SJL

hematopoietic system

decreased thymocyte number ( J:132114 )

• an 80-90% reduction compared to control showing no rescue of the reduced thymic cellularity resulting from Cops5 deficiency

immune system

decreased thymocyte number ( J:132114 )

• an 80-90% reduction compared to control showing no rescue of the reduced thymic cellularity resulting from Cops5 deficiency

endocrine/exocrine glands

decreased thymocyte number ( J:132114 )

• an 80-90% reduction compared to control showing no rescue of the reduced thymic cellularity resulting from Cops5 deficiency

Genotype
MGI:6260011

cn32

• Allelic Composition: Rps6^tm1Gtho/Rps6⁺; Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(KRT5-cre)5132Jlj/0
• Genetic Background: involves: 129 * C57BL/6J * DBA/2J

pigmentation

pigmentation phenotype ( J:139244 )

N • mice exhibit normal footpad pigmentation and normal Kitl mRNA levels in the footpad epidermis at P30, indicating complete reversal of the phenotype observed in mice that are only heterozygous for Rps6^tm1Gtho and hemizygous for Tg(KRT5-cre)5132Jlj

Genotype
MGI:6260013

cn33

• Allelic Composition: Rps6^tm1Gtho/Rps6⁺; Trp53^tm1Tyj/Trp53⁺; Tg(KRT5-cre)5132Jlj/0
• Genetic Background: involves: 129 * C57BL/6J * DBA/2J

pigmentation

increased foot pad pigmentation ( J:139244 )

• mice exhibit an intermediate footpad pigmentation phenotype and reduced Kitl mRNA levels in the footpad epidermis at P30, indicating partial amelioration of the dark skin observed in mice that are only heterozygous for Rps6^tm1Gtho and hemizygous for Tg(KRT5-cre)5132Jlj

integument

increased foot pad pigmentation ( J:139244 )

• mice exhibit an intermediate footpad pigmentation phenotype and reduced Kitl mRNA levels in the footpad epidermis at P30, indicating partial amelioration of the dark skin observed in mice that are only heterozygous for Rps6^tm1Gtho and hemizygous for Tg(KRT5-cre)5132Jlj

limbs/digits/tail

increased foot pad pigmentation ( J:139244 )

• mice exhibit an intermediate footpad pigmentation phenotype and reduced Kitl mRNA levels in the footpad epidermis at P30, indicating partial amelioration of the dark skin observed in mice that are only heterozygous for Rps6^tm1Gtho and hemizygous for Tg(KRT5-cre)5132Jlj

Genotype
MGI:3831342

cn34

• Allelic Composition: Brca2^tm1Brn/Brca2^tm1Brn; Ptch1^tm1Mps/Ptch1⁺; Trp53^tm1Tyj/Trp53⁺; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129 * C57BL/6 * SJL

neoplasm

increased medulloblastoma incidence ( J:144617 )

• 100% of mice develop medulloblastoma beginning at 10 weeks

nervous system

increased medulloblastoma incidence ( J:144617 )

• 100% of mice develop medulloblastoma beginning at 10 weeks

Genotype
MGI:3831343

cn35

• Allelic Composition: Brca2^tm1Brn/Brca2^tm1Brn; Ptch1^tm1Mps/Ptch1⁺; Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129 * C57BL/6 * SJL

neoplasm

increased medulloblastoma incidence ( J:144617 )

• 100% of mice develop medulloblastoma beginning at 5 weeks

nervous system

increased medulloblastoma incidence ( J:144617 )

• 100% of mice develop medulloblastoma beginning at 5 weeks

Genotype
MGI:3710322

cn36

• Allelic Composition: Cdkn2c^tm1Bbd/Cdkn2c^tm1Bbd; Trp53^tm1Brn/Trp53^tm1Tyj; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL

neoplasm

increased medulloblastoma incidence ( J:102702 )

• 4/4 of mice receiving 4 Gy radiation at P5 develop cerebellar tumors by 5 months of age

nervous system

increased medulloblastoma incidence ( J:102702 )

• 4/4 of mice receiving 4 Gy radiation at P5 develop cerebellar tumors by 5 months of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
medulloblastoma		DOID:0050902	OMIM:155255	J:102702

Genotype
MGI:5553372

cn37

• Allelic Composition: Nle1^tm1Cba/Nle1^tm1.1Cota; Gt(ROSA)26Sor^{tm2(cre/ERT2)Brn}/Gt(ROSA)26Sor⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas

hematopoietic system

hematopoietic system phenotype ( J:204063 )

N • tamoxifen-treated mice exhibit rescued total bone marrow and LSK cells

Genotype
MGI:4948964

cn38

• Allelic Composition: Kras^tm4Tyj/Kras⁺; Map2k7^tm1.1Twad/Map2k7^tm1.2Twad; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6

neoplasm

increased lung tumor incidence ( J:170904 )

• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice

• however, tumorigenesis is the same as in Map2k7^tm1.1Twad/Map2k7^tm1.2Twad Kras^tm4Tyj/Kras⁺ mice

increased lung adenocarcinoma incidence ( J:170904 )

• following adenovirus cre infection, mice exhibit more adenocarcinomas than Map2k7^tm1.1Twad/Map2k7^tm1.2Twad Kras^tm4Tyj/Kras⁺ mice

respiratory system

increased lung tumor incidence ( J:170904 )

• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice

• however, tumorigenesis is the same as in Map2k7^tm1.1Twad/Map2k7^tm1.2Twad Kras^tm4Tyj/Kras⁺ mice

increased lung adenocarcinoma incidence ( J:170904 )

• following adenovirus cre infection, mice exhibit more adenocarcinomas than Map2k7^tm1.1Twad/Map2k7^tm1.2Twad Kras^tm4Tyj/Kras⁺ mice

Genotype
MGI:3767597

cn39

• Allelic Composition: Fbxw7^tm1Kei/Fbxw7^tm1Kei; Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(Lck-cre)1Cwi/?
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

neoplasm

increased lymphoma incidence ( J:128523 )

• mice develop double positive lymphomas at increased frequency and decreased latency compared to Fbxw7^tm1Kei/Fbxw7^tm1Kei Tg(Lck-cre)1Cwi mice

increased T cell derived lymphoma incidence ( J:128523 )

• at 8 weeks of age 2 mice develop thymic lymphoma

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:128523 )

• at 8 weeks of age 2 mice develop thymic lymphoma

immune system

immune system phenotype ( J:128523 )

N • unlike in Fbxw7^tm1Kei/Fbxw7^tm1Kei Tg(Lck-cre)1Cwi mice, T cells do not arrest in S phase or undergo increased apoptosis

Genotype
MGI:6505488

cn40

• Allelic Composition: Atrip^tm1.1Pof/Atrip^tm1.1Pof; Tg(Pax6-cre,GFP)2Pgr/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

vision/eye

vision/eye phenotype ( J:297493 )

N • retinas show normal morphology, lamination, and an intact outer nuclear layer, and mice exhibit a normal optomotor response

N • mice show rescue of the increased apoptosis seen in the retinas of single homozygous Atrip conditional mice

Genotype
MGI:5906184

cn41

• Allelic Composition: Nop53^tm2.1Asuz/Nop53^tm2.1Asuz; Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(Lck-cre)#Jxm/0
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * CBA

endocrine/exocrine glands

decreased thymocyte number ( J:241062 )

• Trp53 KO rescues thymocyte reducing phenotype of Nop53 KO

hematopoietic system

decreased thymocyte number ( J:241062 )

• Trp53 KO rescues thymocyte reducing phenotype of Nop53 KO

immune system

decreased thymocyte number ( J:241062 )

• Trp53 KO rescues thymocyte reducing phenotype of Nop53 KO

Genotype
MGI:3710323

cn42

• Allelic Composition: Trp53^tm1Brn/Trp53^tm1Tyj; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL

neoplasm

increased medulloblastoma incidence ( J:102702 )

• 2/5 (40%) of mice receiving 4 Gy radiation at P5 develop cerebellar tumors by 5 months of age

nervous system

increased medulloblastoma incidence ( J:102702 )

• 2/5 (40%) of mice receiving 4 Gy radiation at P5 develop cerebellar tumors by 5 months of age

Genotype
MGI:3698834

cn43

• Allelic Composition: Ddb1^tm1Spg/Ddb1^tm1Spg; Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL

mortality/aging

neonatal lethality, complete penetrance ( J:117820 )

• mutants do not survive for more than a day

nervous system

abnormal brain morphology ( J:117820 )

• ventricular zone (VZ) and subventricular zone (SVZ) are irregularly enlarged with many abnormal cells; cells show high frequency of mitotic figures, apoptosis and irregularly shaped nuclei

vision/eye

abnormal lens epithelium morphology ( J:117820 )

• loss of lens epithelium cells is rescued compared to Ddb1^tm1Spg;Tg(Nes-cre)1Kln mice; however, cells have abnormally large or small nuclei with irregular shapes and sporadic apoptosis

Genotype
MGI:3831340

cn44

• Allelic Composition: Brca2^tm1Brn/Brca2^tm1Brn; Trp53^tm1Tyj/Trp53⁺; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL

neoplasm

abnormal tumor morphology ( J:144617 )

• tumors exhibit a loss of heterozygosity at the Trp53 gene

increased medulloblastoma incidence ( J:144617 )

• 72% of mice develop medulloblastoma beginning at 21 weeks

nervous system

increased medulloblastoma incidence ( J:144617 )

• 72% of mice develop medulloblastoma beginning at 21 weeks

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
medulloblastoma		DOID:0050902	OMIM:155255	J:144617

Genotype
MGI:3831341

cn45

• Allelic Composition: Brca2^tm1Brn/Brca2^tm1Brn; Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL

neoplasm

increased medulloblastoma incidence ( J:144617 )

• 87% of mice develop medulloblastoma beginning at 13 weeks

nervous system

increased medulloblastoma incidence ( J:144617 )

• 87% of mice develop medulloblastoma beginning at 13 weeks

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
medulloblastoma		DOID:0050902	OMIM:155255	J:144617

Genotype
MGI:3710239

cn46

• Allelic Composition: Rb1^tm1Tyj/Rb1^tm2Brn; Rbl1^tm1Tyj/Rbl1^tm1Tyj; Trp53^tm1Brn/Trp53^tm1Tyj; Tg(Chx10-EGFP/cre,-ALPP)2Clc/0
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL

vision/eye

increased retinoblastoma incidence ( J:120315 )

• retinoblastoma cells that express amacrine/horizontal cell markers also extend processes and form synapses; some of these Golgi-Cox-labeled cells extend 1-3 long main processes with further neurite branching characteristic of horizontal or wide-field amacrine cells, while more (nearly half of ) labeled cells extend a main process with extensive neurite outgrowth characteristic of amacrine cells, and the remaining cells are less differentiated with short, unbranched neurites

• these labeled cells are mainly found near the tumor origin, while fewer are present toward the lens and anterior chamber

abnormal eye anterior chamber morphology ( J:120315 )

• tumor cells that invade the anterior eye chamber beneath the cornea are densely packed stage II cells surrounded by sparse regions of plexus with no synaptic densities or vesiclesin in the plexus or rosettes of these cells

• tumor cells have abundant mitochondria and mitotic figures; some rosettes have a central plexus made up of large, undifferentiated processes, with other rosettes having a central plexus containing neurons and synapses

abnormal eye posterior chamber morphology ( J:120315 )

• areas of the plexus within the posterior chamber are composed of neuron-like processes having synaptic structures similar to horizontal/amacrine cells; this is seen in extensive plexus areas of tumors

neoplasm

increased retinoblastoma incidence ( J:120315 )

• retinoblastoma cells that express amacrine/horizontal cell markers also extend processes and form synapses; some of these Golgi-Cox-labeled cells extend 1-3 long main processes with further neurite branching characteristic of horizontal or wide-field amacrine cells, while more (nearly half of ) labeled cells extend a main process with extensive neurite outgrowth characteristic of amacrine cells, and the remaining cells are less differentiated with short, unbranched neurites

• these labeled cells are mainly found near the tumor origin, while fewer are present toward the lens and anterior chamber

cellular

abnormal cell proliferation ( J:120315 )

• a substantial proportion of tumor cells expressing amacrine/horizontal cell markers are proliferating as shown by labeled thymidine incorporation

Genotype
MGI:5907135

cn47

• Allelic Composition: Mdm4^tm2Glo/Mdm4^tm2.1Glo; Tg(Myh6-cre)2182Mds/0; Trp53^tm1Tyj/Trp53^tm1Brn
• Genetic Background: involves: 129P2/OlaHsd * 129S/Sv * C57BL/6J * FVB/N

mortality/aging

decreased tumor-free survival time ( J:137114 )

• mice die due to tumors not heart failure

extended life span ( J:137114 )

• mice show an extended mean survival of 403 days compared to compound heterozygous Mdm4^tm2Glo/Mdm4^tm2.1Glo conditional mutants

cardiovascular system

cardiovascular system phenotype ( J:137114 )

N • mice do not exhibit signs of heart failure such as edema and poor breathing and exhibit rescue of the dilated cardiomyopathy

neoplasm

increased tumor incidence ( J:137114 )

Genotype
MGI:4840094

cn48

• Allelic Composition: Nf1^tm1Par/Nf1⁺; Pten^tm1Hwu/Pten⁺; Trp53^tm1Tyj/Trp53⁺; Tg(GFAP-cre)25Mes/0
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * 129S4/SvJae * 129X1/SvJ * FVB/N

mortality/aging

premature death ( J:134611 )

• most die as early as 10 weeks of age, and usually within a week of showing signs of morbidity

behavior/neurological

increased startle reflex ( J:134611 )

• exaggerated startle response

ataxia ( J:134611 )

• ataxic gait

unidirectional circling ( J:134611 )

seizures ( J:134611 )

• generalized motor seizures

nervous system

seizures ( J:134611 )

• generalized motor seizures

increased brain tumor incidence ( J:134611 )

increased astrocytoma incidence ( J:134611 )

• gliomas from asymptomatic mutants are primarily classified as grade 3 astocytomas

• 5-fold higher growth rate of astrocytomas compared with tumors from transgenic mice heterozygous for Nf1^tm1Par and Trp53^tm1Tyj and hemizygous for Tg(GFAP-cre)25Mes

neoplasm

increased brain tumor incidence ( J:134611 )

increased astrocytoma incidence ( J:134611 )

• gliomas from asymptomatic mutants are primarily classified as grade 3 astocytomas

• 5-fold higher growth rate of astrocytomas compared with tumors from transgenic mice heterozygous for Nf1^tm1Par and Trp53^tm1Tyj and hemizygous for Tg(GFAP-cre)25Mes

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
malignant astrocytoma		DOID:3069		J:134611

Genotype
MGI:6887493

cn49

• Allelic Composition: Taf1b^{tm1c(EUCOMM)Hmgu}/Taf1b^{tm1c(EUCOMM)Hmgu}; Trp53^tm1Tyj/Trp53^tm1Tyj; Gt(ROSA)26Sor^{tm1(cre/ERT)Nat}/Gt(ROSA)26Sor^{tm1(cre/ERT)Nat}
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6J * C57BL/6N
• Cell Lines: HEPD0596_3_G02

cellular

abnormal nucleolus morphology ( J:321558 )

• tamoxifen treated MEFs exhibit disruption of nucleolar structure characteristic of nucleolar stress

Genotype
MGI:5569005

cn50

• Allelic Composition: Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy}/Gt(ROSA)26Sor⁺; Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺; Tg(tetO-Kras2)12Hev/0; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6J * FVB/N

mortality/aging

premature death ( J:184378 )

• mice die between 8 and 18 weeks after doxycycline (dox) treatment to induce Kras2 expression due to pancreatic ductal adenocarinoma

neoplasm

increased pancreatic ductal adenocarcinoma incidence ( J:184378 )

• mice develop invasive adenocarcinoma between 8 and 18 weeks after dox treatment, with some cases showing hemorrhagic ascites, with admixed poorly differentiated and well-differentiated areas and duodenal invasion

• mice in which dox is removed recover their health and show pancreatic tumor regression resulting in a small pancreatic remnant

increased pancreatic intraepithelial neoplasia incidence ( J:184378 )

• adult mice treated with dox 72 hours prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis develop PanINs, dilated ducts with the presence of intracellular mucins, and extensive fibroinflammatory stroma

homeostasis/metabolism

increased susceptibility to injury ( J:184378 )

• adult mice treated with dox for 5 weeks prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis exhibit a small, translucent remnant of pancreatic tissue, without fibrosis or PanIN lesions

• when dox is removed after pancreatitis induction, mice show show normal acini interspersed with dilated ducts and acinar-ductal metaplasia, fibrosis and occasional lipomatosis, but with minimal inflammatory infiltrate, and reduced proliferation

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:184378 )

• mice develop invasive adenocarcinoma between 8 and 18 weeks after dox treatment, with some cases showing hemorrhagic ascites, with admixed poorly differentiated and well-differentiated areas and duodenal invasion

• mice in which dox is removed recover their health and show pancreatic tumor regression resulting in a small pancreatic remnant

increased pancreatic intraepithelial neoplasia incidence ( J:184378 )

• adult mice treated with dox 72 hours prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis develop PanINs, dilated ducts with the presence of intracellular mucins, and extensive fibroinflammatory stroma

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
pancreatic carcinoma		DOID:4905	OMIM:260350	J:184378

Genotype
MGI:4840090

cn51

• Allelic Composition: Nf1^tm1Par/Nf1⁺; Trp53^tm1Tyj/Trp53⁺; Tg(GFAP-cre)25Mes/0
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * FVB/N

mortality/aging

premature death ( J:134611 )

• mutants survive up to 8 weeks beyond initial appearance of symptoms

neoplasm

increased brain tumor incidence ( J:134611 )

increased astrocytoma incidence ( J:134611 )

• complete penetrance of malignant astrocytomas

• gliomas from asymptomatic mutants are primarily classified as grade 2 astocytomas

• neurospheres from mutant astrocytomas exhibit loss of heterozygosity at both Nf1 and Trp53 loci

nervous system

increased brain tumor incidence ( J:134611 )

increased astrocytoma incidence ( J:134611 )

• complete penetrance of malignant astrocytomas

• gliomas from asymptomatic mutants are primarily classified as grade 2 astocytomas

• neurospheres from mutant astrocytomas exhibit loss of heterozygosity at both Nf1 and Trp53 loci

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
malignant astrocytoma		DOID:3069		J:134611

Genotype
MGI:3831348

cn52

• Allelic Composition: Lig4^tm1Pmc/Lig4^tm1Pmc; Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL

mortality/aging

premature death ( J:144617 )

• mice die by 32 weeks unlike Lig4^tm1Pmc/Lig4^tm1Pmc Tg(Nes-cre)1Kln mice with wild-type Trp53

neoplasm

increased medulloblastoma incidence ( J:144617 )

• 94% of mice develop medulloblastoma beginning at 16 weeks

nervous system

increased medulloblastoma incidence ( J:144617 )

• 94% of mice develop medulloblastoma beginning at 16 weeks

Genotype
MGI:3831338

cn53

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Xrcc2^tm2Pmc/Xrcc2^tm2Pmc; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL

mortality/aging

premature death ( J:144617 )

• mice die by 28 weeks unlike Xrcc2^tm2Pmc/Xrcc2^tm2Pmc Tg(Nes-cre)1Kln mice with wild-type Trp53

neoplasm

increased medulloblastoma incidence ( J:144617 )

• 100% of mice develop medulloblastoma beginning at 16 weeks

nervous system

increased medulloblastoma incidence ( J:144617 )

• 100% of mice develop medulloblastoma beginning at 16 weeks

Genotype
MGI:4359665

cn54

• Allelic Composition: Xrcc1^tm1Pmc/Xrcc1^tm1Pmc; Trp53^tm1Tyj/Trp53⁺; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL

mortality/aging

premature death ( J:152528 )

• mice die by 6 months of age

neoplasm

increased medulloblastoma incidence ( J:152528 )

• in 13% of mice

nervous system

increased medulloblastoma incidence ( J:152528 )

• in 13% of mice

Genotype
MGI:3831351

cn55

• Allelic Composition: Lig4^tm1Pmc/Lig4^tm1Pmc; Trp53^tm1Tyj/Trp53^tm1Tyj; Xrcc2^tm2Pmc/Xrcc2^tm2Pmc; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL

mortality/aging

premature death ( J:144617 )

• mice die by 16 weeks

neoplasm

increased medulloblastoma incidence ( J:144617 )

• 100% of mice develop medulloblastoma beginning at 14 weeks

nervous system

increased medulloblastoma incidence ( J:144617 )

• 100% of mice develop medulloblastoma beginning at 14 weeks

Genotype
MGI:4359666

cn56

• Allelic Composition: Xrcc1^tm1Pmc/Xrcc1^tm1Pmc; Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL

mortality/aging

premature death ( J:152528 )

• mice die by 4 months of age

nervous system

nervous system phenotype ( J:152528 )

N • loss of interneurons in the molecular layer of the cerebellum observed in Xrcc1^tm1.1Pmc/Xrcc1^tm1.1Pmc Tg(Nes-cre)1Kln is rescued with normal distribution of basket and stellate cells

abnormal neuron differentiation ( J:152528 )

• Golgi cells are only partially rescued compared to in Xrcc1^tm1.1Pmc/Xrcc1^tm1.1Pmc Tg(Nes-cre)1Kln

increased medulloblastoma incidence ( J:152528 )

neoplasm

increased medulloblastoma incidence ( J:152528 )

cellular

abnormal neuron differentiation ( J:152528 )

• Golgi cells are only partially rescued compared to in Xrcc1^tm1.1Pmc/Xrcc1^tm1.1Pmc Tg(Nes-cre)1Kln

Genotype
MGI:3831355

cn57

• Allelic Composition: Lig4^tm1Pmc/Lig4^tm1Pmc; Trp53^tm1Tyj/Trp53⁺; Xrcc2^tm2Pmc/Xrcc2^tm2Pmc; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL

mortality/aging

premature death ( J:144617 )

• mice die by 32 weeks

neoplasm

abnormal tumor morphology ( J:144617 )

• tumors exhibit a loss of heterozygosity at the Trp53 gene

increased medulloblastoma incidence ( J:144617 )

• 75% of mice develop medulloblastoma beginning at 23 weeks

nervous system

increased medulloblastoma incidence ( J:144617 )

• 75% of mice develop medulloblastoma beginning at 23 weeks

Genotype
MGI:5305073

cn58

• Allelic Composition: Gt(ROSA)26Sor^{tm1(cre/ERT2)Tyj}/Gt(ROSA)26Sor⁺; Tacc3^tm1.1Tno/Tacc3^tm1.2Tno; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * C57BL/6

neoplasm

increased T cell derived lymphoma incidence ( J:179414 )

• in the absence of 4OHT, mutants develop thymic lymphoma tumors

decreased lymphoma incidence ( J:179414 )

• administration of 4-hydroxytamoxifen (4OHT) to induce Cre recombination results in regression of autochthonous thymic lymphoma, with a reduction in tumor volume to 96% and 26% of original volume, over 3 and 10 days, respectively

• regression of tumors is due to apoptosis in thymic lymphoma

• 4OHT treatment of mutants results in massive apoptosis in thymic lymphomas but not in normal thymic tissue or other tissues

• lymphoma cells contain multi-polar spindles, indicating aberrant spindle formation, resulting in mitotic arrest and rapid cell death

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:179414 )

• in the absence of 4OHT, mutants develop thymic lymphoma tumors

Genotype
MGI:5305074

cn59

• Allelic Composition: Gt(ROSA)26Sor^{tm1(cre/ERT2)Tyj}/Gt(ROSA)26Sor⁺; Tacc3^tm1.1Tno/Tacc3⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * C57BL/6

neoplasm

increased T cell derived lymphoma incidence ( J:179414 )

• administration of 4-hydroxytamoxifen (4OHT) to induce Cre recombination results in a rapid increase in tumor volume

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:179414 )

• administration of 4-hydroxytamoxifen (4OHT) to induce Cre recombination results in a rapid increase in tumor volume

Genotype
MGI:4836239

cn60

• Allelic Composition: Pten^tm1Hwu/Pten^tm1Hwu; Tg(Pdx1-cre)89.1Dam/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 * CBA

neoplasm

increased pancreatic acinar cell carcinoma incidence ( J:102226 )

• 1 of 5 mutants develop a small acinar carcinoma

increased pancreatic ductal adenocarcinoma incidence ( J:102226 )

• 2 of 5 mutants develop papillary adenocarcionomas at 4 and 6 months of age

endocrine/exocrine glands

increased pancreatic acinar cell carcinoma incidence ( J:102226 )

• 1 of 5 mutants develop a small acinar carcinoma

increased pancreatic ductal adenocarcinoma incidence ( J:102226 )

• 2 of 5 mutants develop papillary adenocarcionomas at 4 and 6 months of age

Genotype
MGI:3849178

cn61

• Allelic Composition: Trp53^tm1Elee/Trp53^tm1Tyj; Tg(GFAP-cre)25Mes/0
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * FVB/N

mortality/aging

premature death ( J:149662 )

• all mice die prior to 500 days

behavior/neurological

tremors ( J:149662 )

• 85% of mice

ataxia ( J:149662 )

• 85% of mice

impaired balance ( J:149662 )

• 85% of mice

seizures ( J:149662 )

• 85% of mice

neoplasm

increased medulloblastoma incidence ( J:149662 )

• 90% of mice develop medulloblastomas

increased sarcoma incidence ( J:149662 )

• mice develop tumors outside of the central nervous system consisting of soft-tissue sarcomas

increased glioma incidence ( J:149662 )

• 90% of mice develop malignant gliomas with astrocytic characteristics

• 40% of high-grade astrocytic gliomas exhibit necrosis, pseudopalisading tumors cells, high degree of nuclear atypia, and microvascular proliferation similar to human glioblastoma multiforme

• tumors are relatively heterogeneous histological and in lineage marker expression

nervous system

nervous system phenotype ( J:149662 )

N • at 2 months of age, brain cells in the subventricular zone and progenitor cells exhibit normal growth rates

seizures ( J:149662 )

• 85% of mice

increased medulloblastoma incidence ( J:149662 )

• 90% of mice develop medulloblastomas

increased glioma incidence ( J:149662 )

• 90% of mice develop malignant gliomas with astrocytic characteristics

• 40% of high-grade astrocytic gliomas exhibit necrosis, pseudopalisading tumors cells, high degree of nuclear atypia, and microvascular proliferation similar to human glioblastoma multiforme

• tumors are relatively heterogeneous histological and in lineage marker expression

increased brain size ( J:149662 )

• in mice with neurological defects

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
glioblastoma		DOID:3068		J:149662

Genotype
MGI:3783529

cn62

• Allelic Composition: Rb1^tm3Tyj/Rb1^tm3Tyj; Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(Nes-cre)1Atp/0
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * FVB/N

mortality/aging

decreased tumor-free survival time ( J:91406 )

• mice with mosaic cre expression due to maternal inheritance of Tg(Nes-cre)1Mrt exhibit an average lifespan of 92+/-15 days and are moribund with pituitary tumors when euthanized

endocrine/exocrine glands

increased pituitary gland tumor incidence ( J:91406 )

• mice with mosaic cre expression with maternal inheritance of Tg(Nes-cre)1Mrt exhibit pituitary tumors

vision/eye

increased retina apoptosis ( J:91406 )

• retinal apoptosis levels are higher than in wild-type and Rb1^tm3Tyj/Rb1^tm3Tyj Tg(Nes-cre)1Mrt mice

abnormal eye morphology ( J:91406 )

• dysplasia in both eyes

abnormal retina morphology ( J:91406 )

• mice with mosaic cre expression due to maternal inheritance of Tg(Nes-cre)1Mrt exhibit focal retinal dysplasia

decreased retina photoreceptor cell number ( J:91406 )

thin retina outer nuclear layer ( J:91406 )

• in mice with mosaic cre expression when Tg(Nes-cre)1Mrt is maternally inherited

neoplasm

increased pituitary gland tumor incidence ( J:91406 )

• mice with mosaic cre expression with maternal inheritance of Tg(Nes-cre)1Mrt exhibit pituitary tumors

nervous system

increased pituitary gland tumor incidence ( J:91406 )

• mice with mosaic cre expression with maternal inheritance of Tg(Nes-cre)1Mrt exhibit pituitary tumors

decreased retina photoreceptor cell number ( J:91406 )

cellular

increased retina apoptosis ( J:91406 )

• retinal apoptosis levels are higher than in wild-type and Rb1^tm3Tyj/Rb1^tm3Tyj Tg(Nes-cre)1Mrt mice

Genotype
MGI:5907132

cn63

• Allelic Composition: Mdm4^tm2Glo/Mdm4^tm2.1Glo; Tg(Myh6-cre)2182Mds/0; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJaeSor * 129S7/SvEvBrd * C57BL/6J * FVB/N

mortality/aging

extended life span ( J:137114 )

• mice show an extended median survival of 274 days compared to compound heterozygous Mdm4^tm2Glo/Mdm4^tm2.1Glo conditional mutants

Genotype
MGI:5526849

cn64

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Usp7^tm2Wgu/Usp7^tm2Wgu; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * SJL

mortality/aging

neonatal lethality, complete penetrance ( J:203102 )

nervous system

nervous system phenotype ( J:203102 )

N • mice exhibit normal forebrain, midbrain and cerebellum size, cerebellum thickness and neural cell density

open neural tube ( J:203102 )

• in some mice

embryo

open neural tube ( J:203102 )

• in some mice

Genotype
MGI:3616710

cn65

• Allelic Composition: Mdm2^tm1Glo/Mdm2^tm2.1Glo; Tg(Myh6-cre)2182Mds/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * FVB/N

cardiovascular system

cardiovascular system phenotype ( J:104114 )

N • exhibit rescue of the heart lethality seen in conditional Mdm2 mice and have the same life span as single homozygous Trp53 mice

Genotype
MGI:5317026

cn66

• Allelic Composition: Tg(Atoh1-sb11)1Mtay/0; TgTn(sb-T2/Onc3)12740Njen/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C3H * C57BL/6J * ICR

neoplasm

increased medulloblastoma incidence ( J:181542 )

• in some mice with large cells, nuclear atypia and nuclear moulding typical of large cell/anaplastic histology

nervous system

increased medulloblastoma incidence ( J:181542 )

• in some mice with large cells, nuclear atypia and nuclear moulding typical of large cell/anaplastic histology

Genotype
MGI:6515759

cn67

• Allelic Composition: Alb^{tm1(cre/ERT2)Mtz}/Alb⁺; Polr2m^tm1.1Rgr/Polr2m^tm1.1Rgr; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

liver/biliary system

increased hepatocyte karyomegaly ( J:291184 )

• following tamoxifen injection, nuclei are enlarged compared to cells from Trp53 null mice

increased hepatocyte proliferation ( J:291184 )

• expression analysis indicates hepatocytes rapidly reenter the cell cycle after tamoxifen treatment

cellular

increased hepatocyte karyomegaly ( J:291184 )

• following tamoxifen injection, nuclei are enlarged compared to cells from Trp53 null mice

increased hepatocyte proliferation ( J:291184 )

• expression analysis indicates hepatocytes rapidly reenter the cell cycle after tamoxifen treatment

Genotype
MGI:6515760

cn68

• Allelic Composition: Polr2m^tm1.1Rgr/Polr2m^tm1.1Rgr; Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * DBA

liver/biliary system

increased hepatocyte apoptosis ( J:291184 )

• dramatically increased by 8 weeks of age

increased hepatocyte proliferation ( J:291184 )

• expression analysis indicates more cells have re-entered the cell cycle and at 8 weeks of age the number of Ki67 positive hepatocytes is further increased

abnormal liver morphology ( J:291184 )

• liver architecture is distorted with the pericentral expression pattern of glutamine synthetase absent

abnormal hepatocyte morphology ( J:291184 )

• increased size with some being extremely enlarged and containing more than 3 nuclei indicating incomplete mitoses

cellular

increased hepatocyte apoptosis ( J:291184 )

• dramatically increased by 8 weeks of age

increased hepatocyte proliferation ( J:291184 )

• expression analysis indicates more cells have re-entered the cell cycle and at 8 weeks of age the number of Ki67 positive hepatocytes is further increased

Genotype
MGI:5292118

cn69

• Allelic Composition: Tg(EIIa-cre)C5379Lmgd/0; Tg(Rnu6-RNAi:Bccip)4Zshn/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB/N

mortality/aging

embryonic lethality ( J:176115 )

• Trp53 deficiency does not result in significant rescue of the embryonic lethality seen in Bccip deficiency; ratio of viable double transgenic to wild-type offspring is not increased in the Trp53-null or heterozygous background

Genotype
MGI:3044602

cn70

• Allelic Composition: Tg(ACTB-NOTCH1)1Shn/0; Tg(Nes-cre)1Kln/0; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

cellular

abnormal apoptosis ( J:90392 )

• at E10 - 11.5 the number of apoptotic cells in the brain is increased

Genotype
MGI:3044601

cn71

• Allelic Composition: Tg(ACTB-NOTCH1)1Shn/0; Tg(Nes-cre)1Kln/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

mortality/aging

prenatal lethality, incomplete penetrance ( J:90392 )

• fewer than expected double transgenic homozygous mutants are found due to incomplete penetrance of Trp53^tm1Tyj embryonic lethality

cellular

cellular phenotype ( J:90392 )

N • at E10 - 11.5 no increase in the number of apoptotic cells in the brain is found unlike in double transgenics with wild-type Trp53

Genotype
MGI:6192377

cn72

• Allelic Composition: Kdm6a^tm1Cdcn/Y; Tg(CAG-cre/Esr1*)5Amc/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6J * CBA * FVB/N

mortality/aging

premature death ( J:263565 )

• tamoxifen-treated mice have a median survival of 3.8 months

neoplasm

increased chronic myelocytic leukemia incidence ( J:263565 )

• tamoxifen treated mice develop chronic myelomonocytic leukemia-like disease with a shorter latency than single Kdm6a mutants

hematopoietic system

enlarged spleen ( J:263565 )

• splenomegaly develops 3 months after tamoxifen injection

anemia ( J:263565 )

• in tamoxifen treated mice

increased granulocyte monocyte progenitor cell number ( J:263565 )

• increase in number of granulocyte-macrophage progenitor (GMP) cells in the bone marrow of tamoxifen treated mice

decreased erythrocyte cell number ( J:263565 )

• decrease in number of red blood cells in tamoxifen treated mice which is greater than in either single mutant

increased neutrophil cell number ( J:263565 )

• expansion of neutrophils in the spleen, bone marrow, liver and peripheral blood of tamoxifen treated mice

thrombocytopenia ( J:263565 )

• decrease in number of platelets in tamoxifen treated mice which is greater than in either single mutant

increased monocyte cell number ( J:263565 )

• increase in the number of monocytes in tamoxifen treated mice, which is much greater than in either single mutant

increased myeloid cell number ( J:263565 )

• expansion of myeloid cells in the spleen, bone marrow, liver, and peripheral blood of tamoxifen treated mice

increased hematopoietic stem cell number ( J:263565 )

• an increase in the number and proportion of hematopoietic stem cells (HSCs) in the bone marrow of tamoxifen treated mice, however the number of bone marrow cells is normal

immune system

enlarged spleen ( J:263565 )

• splenomegaly develops 3 months after tamoxifen injection

increased neutrophil cell number ( J:263565 )

• expansion of neutrophils in the spleen, bone marrow, liver and peripheral blood of tamoxifen treated mice

increased monocyte cell number ( J:263565 )

• increase in the number of monocytes in tamoxifen treated mice, which is much greater than in either single mutant

growth/size/body

enlarged spleen ( J:263565 )

• splenomegaly develops 3 months after tamoxifen injection

Genotype
MGI:6712734

cn73

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Riok2^{tm1c(KOMP)Wtsi}/Riok2⁺; Commd10^{Tg(Vav1-icre)A2Kio}/Commd10⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6N * C57BL/10 * CBA/Ca

immune system

immune system phenotype ( J:305794 )

N • the increase in IL-22 secretion seen in in vitro polarized TH22 cells in single conditional Riok2 heterozygotes is blunted

Genotype
MGI:7310427

cn74

• Allelic Composition: Rpap3^{tm1c(KOMP)Wtsi}/Rpap3^{tm1c(KOMP)Wtsi}; Tg(Vil1-cre/ERT2)23Syr/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6N * DBA/2

digestive/alimentary system

abnormal small intestine morphology ( J:314346 )

• tamoxifen-treated mice exhibit a delay in epithelium shrinkage compared mice with at least one copy of wild-type Trp53

decreased small intestine length ( J:314346 )

• in tamoxifen-treated mice after 7 days

Genotype
MGI:5316227

cn75

• Allelic Composition: Atr^tm2Bal/Atr^tm2Bal; Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(Nes-cre)1Kln/0
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * SJL

nervous system

abnormal neuron apoptosis ( J:181920 )

• attenuated apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Trp53

• partial rescue of apoptosis in the forebrain compared to mutant mice wild-type for Trp53

abnormal neuron proliferation ( J:181920 )

• substantial enhancement of neurosphere size and growth compared to mutant mice wild-type for Trp53

• however, after 7 days in culture expansion stops and cells fail to survive

abnormal nervous system morphology ( J:181920 )

• similar neuropathology to mutant mice wild-type for Trp53

cellular

abnormal neuron apoptosis ( J:181920 )

• attenuated apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Trp53

• partial rescue of apoptosis in the forebrain compared to mutant mice wild-type for Trp53

abnormal neuron proliferation ( J:181920 )

• substantial enhancement of neurosphere size and growth compared to mutant mice wild-type for Trp53

• however, after 7 days in culture expansion stops and cells fail to survive

Genotype
MGI:3769498

cx76

• Allelic Composition: Rb1^tm1.1Jyjw/Rb1^tm1.1Jyjw; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: 129S6.129-Trp53^tm1Tyj Rb1^tm1.1Jyjw

mortality/aging

premature death ( J:102483 )

• mice become moribund from lymphoma involving various tissues within >30 weeks; mice with aggressive lymphoma have a mean survival time of 18 weeks

digestive/alimentary system

intestinal ulcer ( J:102483 )

• after 7 days of DSS treatment, size of induced ulcers is significantly lower than in Trp53 single mutant littermates

increased colon adenoma incidence ( J:102483 )

• there is a significantly higher incidence of colon tumors in moribund mice with disseminated lymphoma than in Trp53-null single mutant littermates

• tumors have mixture of inflammatory infiltrates within the tumor areas and luminal surface have disrupted epithelial barrier, while colonic tumors

increased intestinal adenocarcinoma incidence ( J:102483 )

• aggressive adenocarcinoma of the colon is observed in double mutants whereas only 1 Trp53 single mutant developed that tumor type; tumors extend through the muscularis mucosa, submucosa, and muscularis, reaching the pericolonic fat

neoplasm

increased colon adenoma incidence ( J:102483 )

• there is a significantly higher incidence of colon tumors in moribund mice with disseminated lymphoma than in Trp53-null single mutant littermates

• tumors have mixture of inflammatory infiltrates within the tumor areas and luminal surface have disrupted epithelial barrier, while colonic tumors

increased intestinal adenocarcinoma incidence ( J:102483 )

• aggressive adenocarcinoma of the colon is observed in double mutants whereas only 1 Trp53 single mutant developed that tumor type; tumors extend through the muscularis mucosa, submucosa, and muscularis, reaching the pericolonic fat

increased lymphoma incidence ( J:102483 )

• mice develop lymphomas, with ~same time of onset and same survival time as Trp53-single mutants

increased teratoma incidence ( J:102483 )

• median survival time of mice with teratomas is 7 weeks compared to 10 weeks for Rb1-sufficient, Trp53-null mice

• higher percentage of teratomas show necrosis with hemorrhage, and are more frequently associated with metastasis than teratomas in Trp53-null single mutant littermates

• ~30% of mice surviving beyond median survival age show extratesticular teratomas in lung, liver, lymph nodes, and/or pancreas

increased testicular teratoma incidence ( J:102483 )

♂ • incidence of testicular tumors is higher than in Trp53 single mutant littermates

cellular

decreased apoptosis ( J:102483 )

• apoptosis of colonic epithelium is lower in double mutants than in Trp53-nulls after treatment with dextran sodium sulfate (DSS) to induce colonic injury

growth/size/body

weight loss ( J:102483 )

• with DSS treatment, double mutants have a reduced average weight loss (loss of 9% body weight) compared to Trp53 single mutants (loss of 14% body weight)

endocrine/exocrine glands

increased testicular teratoma incidence ( J:102483 )

♂ • incidence of testicular tumors is higher than in Trp53 single mutant littermates

reproductive system

increased testicular teratoma incidence ( J:102483 )

♂ • incidence of testicular tumors is higher than in Trp53 single mutant littermates

Genotype
MGI:5286078

cx77

• Allelic Composition: Nf1^tm1Tyj/Nf1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: B6.129S2-Trp53^tm1Tyj Nf1^tm1Tyj/+ +

nervous system

increased glioblastoma incidence ( J:64364 )

increased brain tumor incidence ( J:64364 )

• brain tumors range from diffuse cells with nuclear atypia to glioblastoma multiforme

• Background Sensitivity: mice on a congenic C57BL/6 or C3H/HeJ F1 background develop more brain tumors compared with mice on a CAST/EiJ or SJL/J F1 background

increased astrocytoma incidence ( J:64364 )

mortality/aging

decreased tumor-free survival time ( J:64364 )

• in mice with advanced tumors

neoplasm

increased glioblastoma incidence ( J:64364 )

increased brain tumor incidence ( J:64364 )

• brain tumors range from diffuse cells with nuclear atypia to glioblastoma multiforme

• Background Sensitivity: mice on a congenic C57BL/6 or C3H/HeJ F1 background develop more brain tumors compared with mice on a CAST/EiJ or SJL/J F1 background

increased astrocytoma incidence ( J:64364 )

behavior/neurological

ataxia ( J:64364 )

• in mice with advanced tumors

paralysis ( J:64364 )

• in mice with advanced tumors

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
malignant astrocytoma		DOID:3069		J:64364

Genotype
MGI:5285701

cx78

• Allelic Composition: Espl1^Gt(XL058)Byg/Espl1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: B6.129-Trp53^tm1Tyj Espl1^Gt(XL058)Byg

neoplasm

increased carcinoma incidence ( J:174926 )

• about 50% of mice develop carcinomas over a period of 460 days which is an increased incidence compared to mice heterozygous for the Trp53 mutation alone

Genotype
MGI:5285700

cx79

• Allelic Composition: Espl1^Gt(XL058)Byg/Espl1⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: B6.129-Trp53^tm1Tyj Espl1^Gt(XL058)Byg

mortality/aging

premature death ( J:174926 )

• median survival of 118 day

neoplasm

abnormal tumor pathology ( J:174926 )

• increased levels of proliferation and DNA damage are seen in lung tissue affected by lymphoma

increased metastatic potential ( J:174926 )

• lymphomas are more aggressive and most commonly infiltrate the lungs, liver and spleen with less frequent infiltration of the colon and kidney

increased lymphoma incidence ( J:174926 )

• develop aggressive and widespread lymphomas involving the lung, liver, thymus, bone marrow and peripheral blood with a significantly reduced latency compared to mice null for Trp53 alone

• about 86% of mice develop lymphomas

• seldom localized to the thymus

• most commonly infiltrate the lungs, liver and spleen with less frequent infiltration of the colon and kidney

• lymphoma cells often completely deplete the lungs, liver and spleen completely obscuring the normal anatomy of these tissues

• significant invasion of the bone marrow is seen

increased carcinoma incidence ( J:174926 )

• develop carcinomas in various organs with a significantly reduced latency compared to mice null for Trp53 alone

hematopoietic system

increased splenocyte proliferation ( J:174926 )

• in pre-neoplastic splenocytes

abnormal splenocyte morphology ( J:174926 )

• accumulation of aneuploidy in splenocytes is seen as early as 2.5 months of age

abnormal bone marrow cell physiology ( J:174926 )

• increased proliferation in pre-neoplastic bone marrow cells

cellular

aneuploidy ( J:174926 )

• accumulation of aneuploidy in splenocytes is seen as early as 2.5 months of age

increased splenocyte proliferation ( J:174926 )

• in pre-neoplastic splenocytes

immune system

increased splenocyte proliferation ( J:174926 )

• in pre-neoplastic splenocytes

abnormal splenocyte morphology ( J:174926 )

• accumulation of aneuploidy in splenocytes is seen as early as 2.5 months of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
lymphoma		DOID:0060058		J:174926

Genotype
MGI:5140357

cx80

• Allelic Composition: Rpl27a^Sfa/Rpl27a⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: B6.Cg-Rpl27a^Sfa Trp53^tm1Tyj

behavior/neurological

behavior/neurological phenotype ( J:174216 )

N • motor coordination is similar to Trp53 heterozygous controls

pigmentation

increased foot pad pigmentation ( J:174216 )

hematopoietic system

hematopoietic system phenotype ( J:174216 )

N • no bone marrow deficiencies are detected

nervous system

nervous system phenotype ( J:174216 )

N • no cerebellar deficiencies are detected

integument

increased foot pad pigmentation ( J:174216 )

limbs/digits/tail

increased foot pad pigmentation ( J:174216 )

Genotype
MGI:3639948

cx81

• Allelic Composition: Tert^tm1Rdp/Tert^tm1Rdp; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: B6.Cg-Trp53^tm1Tyj Tert^tm1Rdp

neoplasm

increased incidence of tumors by chemical induction ( J:108914 )

• increased incidence of induced hepatocellular carcinoma after CCl4 treatment in late generation (G3/4) homozygous mice compared to mice with no p53 mutation

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:108914 )

• increased incidence of induced hepatocellular carcinoma after CCl4 treatment in late generation (G3/4) homozygous mice compared to mice with no p53 mutation

Genotype
MGI:5286079

cx82

• Allelic Composition: Nf1^tm1Tyj/Nf1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: (C3H/HeJ x B6.129S2-Trp53^tm1Tyj Nf1^tm1Tyj/+ +)F1

nervous system

increased glioblastoma incidence ( J:64364 )

increased brain tumor incidence ( J:64364 )

• Background Sensitivity: mice on a congenic C57BL/6 or C3H/HeJ F1 background develop more brain tumors compared with mice on a CAST/EiJ or SJL/J F1 background

• brain tumors range from diffuse cells with nuclear atypia to glioblastoma multiforme

increased astrocytoma incidence ( J:64364 )

mortality/aging

decreased tumor-free survival time ( J:64364 )

• in mice with advanced tumors

neoplasm

increased glioblastoma incidence ( J:64364 )

increased brain tumor incidence ( J:64364 )

• Background Sensitivity: mice on a congenic C57BL/6 or C3H/HeJ F1 background develop more brain tumors compared with mice on a CAST/EiJ or SJL/J F1 background

• brain tumors range from diffuse cells with nuclear atypia to glioblastoma multiforme

increased astrocytoma incidence ( J:64364 )

behavior/neurological

ataxia ( J:64364 )

• in mice with advanced tumors

paralysis ( J:64364 )

• in mice with advanced tumors

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
malignant astrocytoma		DOID:3069		J:64364

Genotype
MGI:5286080

cx83

• Allelic Composition: Nf1^tm1Tyj/Nf1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: (CAST/EiJ x B6.129S2-Trp53^tm1Tyj Nf1^tm1Tyj/+ +)F1

nervous system

increased glioblastoma incidence ( J:64364 )

increased brain tumor incidence ( J:64364 )

• brain tumors range from diffuse cells with nuclear atypia to glioblastoma multiforme

• Background Sensitivity: mice on a congenic C57BL/6 or C3H/HeJ F1 background develop more brain tumors compared with mice on a CAST/EiJ or SJL/J F1 background

increased astrocytoma incidence ( J:64364 )

mortality/aging

decreased tumor-free survival time ( J:64364 )

• in mice with advanced tumors

neoplasm

increased glioblastoma incidence ( J:64364 )

increased brain tumor incidence ( J:64364 )

• brain tumors range from diffuse cells with nuclear atypia to glioblastoma multiforme

• Background Sensitivity: mice on a congenic C57BL/6 or C3H/HeJ F1 background develop more brain tumors compared with mice on a CAST/EiJ or SJL/J F1 background

increased astrocytoma incidence ( J:64364 )

behavior/neurological

ataxia ( J:64364 )

• in mice with advanced tumors

paralysis ( J:64364 )

• in mice with advanced tumors

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
malignant astrocytoma		DOID:3069		J:64364

Genotype
MGI:5286081

cx84

• Allelic Composition: Nf1^tm1Tyj/Nf1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: (CBA/J x B6.129S2-Trp53^tm1Tyj Nf1^tm1Tyj/+ +)F1

neoplasm

increased brain tumor incidence ( J:64364 )

nervous system

increased brain tumor incidence ( J:64364 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
malignant astrocytoma		DOID:3069		J:64364

Genotype
MGI:3655296

cx85

• Allelic Composition: Lig4^tm1Icrf/Lig4^tm1Icrf; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: either: (involves: 129P2/OlaHsd * 129S2/SvPas) or (involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ)

neoplasm

increased B cell derived lymphoma incidence ( J:111068 )

• pro-B cell lymphomas develop by 12 weeks of age

increased medulloblastoma incidence ( J:111068 )

• mice develop tumors by 12 weeks of age

nervous system

increased medulloblastoma incidence ( J:111068 )

• mice develop tumors by 12 weeks of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
medulloblastoma		DOID:0050902	OMIM:155255	J:173443

Genotype
MGI:3655297

cx86

• Allelic Composition: Lig4^tm1Icrf/Lig4^tm1Icrf; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: either: (involves: 129P2/OlaHsd * 129S2/SvPas) or (involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ)

mortality/aging

premature death ( J:111068 )

• mice that survive the perinatal period die at ~6 months of age

perinatal lethality, incomplete penetrance ( J:111068 )

• mice are less robust and often die perinatally of indeterminate causes

neoplasm

decreased tumor incidence ( J:111068 )

• mice do not develop tumors before death at 6 months of age

Genotype
MGI:3586556

cx87

• Allelic Composition: Ccne1^tm1Jro/?; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: either: (involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6J) or (involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6 * C57BL/6J)

cellular

increased fibroblast proliferation ( J:99695 )

• cell proliferation in double mutant MEFs is increased compared to MEFs homozygous null for Trp53 alone

neoplasm

decreased tumor latency ( J:99695 )

• mean tumor-free survival is reduced to 145 days compared to 180 days in mice homozygous null for Trp53 alone

Genotype
MGI:4355557

cx88

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Trp63^tm1.1Elrf/Trp63^tm1.1Elrf
• Genetic Background: either: (involves: 129S2/SvPas * C57BL/6 * FVB/N) or (involves: 129S2/SvPas * 129S4/SvJae * 129S6/SvEvTac * C57BL/6)

cellular

early cellular replicative senescence ( J:151638 )

• skin-derived precursors isolated from 1 month old mice exhibit increased staining for a marker of senescence and decreased apoptosis compared with wild-type and Trp63^tm1.1Elrf cells

integument

abnormal skin physiology ( J:151638 )

• after 8 days in culture, epidermal cells form fewer proliferating colonies than wild-type cells but more than Trp63^tm1.1Elrf cells

• after 20 days in culture, epidermal cells fail to form proliferating colonies unlike similarly treated wild-type cells

• skin-derived precursors isolated from 1 month old mice exhibit increased staining for a marker of senescence and decreased apoptosis compared with wild-type and Trp63^tm1.1Elrf cells

Genotype
MGI:3809981

cx89

• Allelic Composition: Nhej1^tm1Fwa/Nhej1^tm1Fwa; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129

neoplasm

increased T cell derived lymphoma incidence ( J:138774 )

• 20 of 21 mice succumbed to thymic lymphoma with a media survival of 102.5 days

• lymphomas characterized lacked clonal translocations suggesting cancers arose from Trp53 deficiency alone

increased B cell derived lymphoma incidence ( J:138774 )

• 1 of 21 mice succumbed to pro-B cell lymphoma

• this lymphoma contained a clonal 12/15 translocation

increased medulloblastoma incidence ( J:138774 )

• necropsy on 8 mice that died from thymic lymphoma revealed 6 of these mice also had medulloblastomas in the brain

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:138774 )

• 20 of 21 mice succumbed to thymic lymphoma with a media survival of 102.5 days

• lymphomas characterized lacked clonal translocations suggesting cancers arose from Trp53 deficiency alone

nervous system

increased medulloblastoma incidence ( J:138774 )

• necropsy on 8 mice that died from thymic lymphoma revealed 6 of these mice also had medulloblastomas in the brain

Genotype
MGI:3759458

cx90

• Allelic Composition: Ptch1^tm1Mps/Ptch1⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129 * 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:125534 )

• mice die around 2 months of age compared to Trp53^tm1Tyj that survive to 5 months

neoplasm

increased rhabdomyosarcoma incidence ( J:125534 )

• 3 of 16 mice develop rhabdomyosarcoma

increased medulloblastoma incidence ( J:125534 )

• 15 of 16 mice develop medulloblastomas that express TUBB3 and GFAP and exhibit increased apoptosis

muscle

increased rhabdomyosarcoma incidence ( J:125534 )

• 3 of 16 mice develop rhabdomyosarcoma

nervous system

increased medulloblastoma incidence ( J:125534 )

• 15 of 16 mice develop medulloblastomas that express TUBB3 and GFAP and exhibit increased apoptosis

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
medulloblastoma		DOID:0050902	OMIM:155255	J:67452

Genotype
MGI:7484076

cx91

• Allelic Composition: Ptprz1^tm1Schl/Ptprz1^tm1Schl; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129 * 129S2/SvPas * C57BL/6J

neoplasm

abnormal tumor pathology ( J:243104 )

• ex vivo, osteosarcoma-derived cell lines exhibit increased proliferation in BrdU incorporation assays, a higher abundance of tyrosine-phosphorylated proteins, and no cellular growth in response to long-term administration of Mdk (midkine, a heparin-binding growth factor known to antagonize Ptprz1 in other cell types)

increased osteosarcoma incidence ( J:243104 )

• at 52 weeks of age, 7 of 38 (~19%) mice exhibit osteosarcoma development by contact X-ray analysis

• skeletal tumors are found in three different locations i.e., ribs, spine or long bones, but not in craniofacial bones, and consist of mineralized tissue

• undecalcified histology showed that tumors represent bony tissue with osteocytes embedded into mineralized matrix, confirming their osteosarcoma nature

• cell lines derived from tumors and cultured in the presence of ascorbic acid and beta-glycerophosphate are able to form a mineralized matrix and show differential expression of osteoblast differentiation markers

skeleton

increased osteosarcoma incidence ( J:243104 )

• at 52 weeks of age, 7 of 38 (~19%) mice exhibit osteosarcoma development by contact X-ray analysis

• skeletal tumors are found in three different locations i.e., ribs, spine or long bones, but not in craniofacial bones, and consist of mineralized tissue

• undecalcified histology showed that tumors represent bony tissue with osteocytes embedded into mineralized matrix, confirming their osteosarcoma nature

• cell lines derived from tumors and cultured in the presence of ascorbic acid and beta-glycerophosphate are able to form a mineralized matrix and show differential expression of osteoblast differentiation markers

Genotype
MGI:7484084

cx92

• Allelic Composition: Ptprz1^tm1Schl/Ptprz1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129 * 129S2/SvPas * C57BL/6J

neoplasm

increased osteosarcoma incidence ( J:243104 )

• at 52 weeks of age, 2 of 38 (~5%) mice exhibit visible skeletal tumors by contact X-ray analysis

• skeletal tumors are found in three different locations i.e., ribs, spine or long bones, but not in craniofacial bones, and consist of mineralized tissue

• cell lines derived from tumors and cultured in the presence of ascorbic acid and beta-glycerophosphate are able to form a mineralized matrix and show differential expression of osteoblast differentiation markers, confirming their osteosarcoma nature

skeleton

increased osteosarcoma incidence ( J:243104 )

• at 52 weeks of age, 2 of 38 (~5%) mice exhibit visible skeletal tumors by contact X-ray analysis

• skeletal tumors are found in three different locations i.e., ribs, spine or long bones, but not in craniofacial bones, and consist of mineralized tissue

• cell lines derived from tumors and cultured in the presence of ascorbic acid and beta-glycerophosphate are able to form a mineralized matrix and show differential expression of osteoblast differentiation markers, confirming their osteosarcoma nature

Genotype
MGI:7484075

cx93

• Allelic Composition: Ptprz1^tm1Schl/Ptprz1^tm1Schl; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129 * 129S2/SvPas * C57BL/6J

neoplasm

neoplasm ( J:243104 )

N • contact Xray and histological analysis of undecalcified spine or tibia sections revealed no signs of osteosarcoma development at 12 weeks of age

Genotype
MGI:3814381

cx94

• Allelic Composition: Kat5^tm1Jwl/Kat5⁺; Tg(IghMyc)22Bri/0; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129 * C57BL * C57BL/6 * SJL

mortality/aging

premature death ( J:125164 )

• mice die prior to 20 weeks of age

neoplasm

increased B cell derived lymphoma incidence ( J:125164 )

• mice exhibit an earlier age of onset and enhanced penetrance of B cell lymphomas compared to in Tg(IghMyc)22Bri mice

Genotype
MGI:2653516

cx95

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Xrcc4^tm1Fwa/Xrcc4^tm1Fwa
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas

mortality/aging

premature death ( J:61973 )

• 3-4 weeks after birth

neoplasm

increased B cell derived lymphoma incidence ( J:61973 )

growth/size/body

postnatal growth retardation ( J:61973 )

hematopoietic system

abnormal lymphopoiesis ( J:61973 )

• impaired lymphocyte development

immune system

abnormal lymphopoiesis ( J:61973 )

• impaired lymphocyte development

Genotype
MGI:4947935

cx96

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺; Xpa^tm1Hvs/Xpa^tm1Hvs
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas

neoplasm

increased incidence of tumors by chemical induction ( J:170769 )

• 22 of 40 mice treated with 2-AAF develop urinary bladder tumors

increased urinary system tumor incidence ( J:170769 )

• 22 of 40 mice treated with 2-AAF develop urinary bladder tumors

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:170769 )

• 22 of 40 mice treated with 2-AAF develop urinary bladder tumors

renal/urinary system

increased urinary system tumor incidence ( J:170769 )

• 22 of 40 mice treated with 2-AAF develop urinary bladder tumors

Genotype
MGI:4420438

cx97

• Allelic Composition: Brca1^tm1Mak/Brca1^tm1Mak; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:41254 )

• mice survive until E9.5

embryo

failure of initiation of embryo turning ( J:41254 )

embryonic growth retardation ( J:41254 )

• at E9.5

decreased embryo size ( J:41254 )

• at E9.5

abnormal allantois morphology ( J:41254 )

abnormal visceral yolk sac morphology ( J:41254 )

growth/size/body

embryonic growth retardation ( J:41254 )

• at E9.5

decreased embryo size ( J:41254 )

• at E9.5

Genotype
MGI:3620761

cx98

• Allelic Composition: Rr149356^tm1Che/Rr149356^tm1Che; Tcrd^tm1Mom/Tcrd^tm1Mom; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6

immune system

abnormal double-negative T cell morphology ( J:106246 )

• most thymocytes are double negative at 4 weeks of age but quickly progress to double positive and then CD8 single positive lymphomas

neoplasm

increased T cell derived lymphoma incidence ( J:106246 )

• most thymocytes are double negative at 4 weeks of age but quickly progress to double positive and then CD8 single positive lymphomas

• mean survival around 14 weeks

hematopoietic system

abnormal double-negative T cell morphology ( J:106246 )

• most thymocytes are double negative at 4 weeks of age but quickly progress to double positive and then CD8 single positive lymphomas

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:106246 )

• most thymocytes are double negative at 4 weeks of age but quickly progress to double positive and then CD8 single positive lymphomas

• mean survival around 14 weeks

Genotype
MGI:4437907

cx99

• Allelic Composition: Igh^tm2Cgn/Igh^tm2Cgn; Igk^tm1Rsky/Igk^tm1Rsky; Trp53^tm1Tyj/Trp53^tm1Tyj; Xrcc4^tm1Fwa/Xrcc4^tm1Fwa
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * 129S6/SvEvTac

immune system

abnormal class switch recombination ( J:126758 )

• class switching to IgG1 is 20% to 50% of wild-type

• class switching to IgG3 is 50% of wild-type

• IgH class switching is reduced compared to in wild-type B cells

cellular

increased cellular sensitivity to ionizing radiation ( J:126758 )

• in cultured B cells

spontaneous chromosome breakage ( J:126758 )

• B cell stimulated with anti-CD40 and IL4 exhibit metaphase chromosome breaks unlike similarly treated wild-type cells

hematopoietic system

abnormal class switch recombination ( J:126758 )

• class switching to IgG1 is 20% to 50% of wild-type

• class switching to IgG3 is 50% of wild-type

• IgH class switching is reduced compared to in wild-type B cells

Genotype
MGI:4437910

cx100

• Allelic Composition: Igh^tm2Cgn/Igh^tm2Cgn; Igk^tm1Rsky/Igk^tm1Rsky; Lig4^tm1Fwa/Lig4^tm1Fwa; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * 129S6/SvEvTac

hematopoietic system

abnormal class switch recombination ( J:126758 )

• class switching to IgG1 in B cells stimulated with anti-CD40 plus IL4 are 50% of wild-type

immune system

abnormal class switch recombination ( J:126758 )

• class switching to IgG1 in B cells stimulated with anti-CD40 plus IL4 are 50% of wild-type

Genotype
MGI:3818475

cx101

• Allelic Composition: Brca2^tm1Kamc/Brca2^tm1Kamc; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * BALB/c * C57BL/6

mortality/aging

decreased survivor rate ( J:109193 )

• 50% survival at 35 weeks of age

• 50% survival at 26 weeks when irradiated with 5Gy

neoplasm

increased stomach tumor incidence ( J:109193 )

• increased incidence of gastric tumors

increased mammary gland tumor incidence ( J:109193 )

• decreased latency for mammary tumor onset

increased osteosarcoma incidence ( J:109193 )

• increased incidence of osteosarcomas

skeleton

increased osteosarcoma incidence ( J:109193 )

• increased incidence of osteosarcomas

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:109193 )

• decreased latency for mammary tumor onset

integument

increased mammary gland tumor incidence ( J:109193 )

• decreased latency for mammary tumor onset

digestive/alimentary system

increased stomach tumor incidence ( J:109193 )

• increased incidence of gastric tumors

Genotype
MGI:3850823

cx102

• Allelic Composition: Igh^{tm2.1(Tag)Rwhe}/Igh⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

neoplasm

increased leukemia incidence ( J:150315 )

• 5 of 6 mice develop B cell derived leukemia compared to Trp53 null controls that develop T cell lymphomas

• median tumor-free survival is 138 days compared to 161 in transgenic controls on a wild-type Trp53 background

increased chronic lymphocytic leukemia incidence ( J:150315 )

Genotype
MGI:5699874

cx103

• Allelic Composition: Nf1^tm1Tyj/Nf1⁺; Suz12^{Gt(Betageo)1Khe}/Suz12⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:217077 )

• mice die by 150 days

neoplasm

increased tumor incidence ( J:217077 )

increased lymphoma incidence ( J:217077 )

• 12% of mice develop lymphomas

increased histiocytic sarcoma incidence ( J:217077 )

• 62% of mice develop histiocytic sarcomas

increased neurofibrosarcoma incidence ( J:217077 )

• 38% of mice develop malignant peripheral nerve sheath tumors

• tumors develop on average at 2.3 months of age

increased hemangiosarcoma incidence ( J:217077 )

• 4% of develop angiosarcomas

increased glioma incidence ( J:217077 )

• 54% of mice develop high-grade gliomas

• gliomas develop on average at 3 months of age

nervous system

increased neurofibrosarcoma incidence ( J:217077 )

• 38% of mice develop malignant peripheral nerve sheath tumors

• tumors develop on average at 2.3 months of age

increased glioma incidence ( J:217077 )

• 54% of mice develop high-grade gliomas

• gliomas develop on average at 3 months of age

Genotype
MGI:5790202

cx104

• Allelic Composition: Cpt1c^Gt(XL823)Byg/Cpt1c⁺; Nf1^tm1Tyj/Nf1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

neoplasm

decreased metastatic potential ( J:228258 )

• mice show a decrease in incidence of metastases compared to double Trp53 and Nf1 heterozygotes, with 19.44% of mice with sarcomas showing metastases compared to 29.4% of double mutants

decreased sarcoma incidence ( J:228258 )

• mice show a decrease in incidence of sarcomas compared to double Trp53 and Nf1 heterozygotes, with 13.89% of mice developing soft tissue sarcomas compared to 59.5% of double mutants

• less proliferation is seen in tumors

immune system

spleen hyperplasia ( J:228258 )

• 25% of mice exhibit splenic hyperplasia

hematopoietic system

spleen hyperplasia ( J:228258 )

• 25% of mice exhibit splenic hyperplasia

growth/size/body

spleen hyperplasia ( J:228258 )

• 25% of mice exhibit splenic hyperplasia

Genotype
MGI:3850824

cx105

• Allelic Composition: Igh^{tm1.1(Tag)Rwhe}/Igh⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

neoplasm

increased leukemia incidence ( J:150315 )

• 4 of 10 mice develop B cell leukemia compared to Trp53 null controls that develop T cell lymphomas

• median tumor-free survival is 143 days compared to over 365 days in transgenic controls on a wild-type Trp53 background

increased chronic lymphocytic leukemia incidence ( J:150315 )

Genotype
MGI:3759457

cx106

• Allelic Composition: Sufu^Gt(XB699)Byg/Sufu⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:125534 )

• mice die around 4 months of age compared to Trp53^tm1Tyj homozygotes that survive to 5 months

neoplasm

increased rhabdomyosarcoma incidence ( J:125534 )

• unlike Sufu^GT(XB699)Byg heterozygotes, 5 of 55 mice develop rhabdomyosarcoma

increased lymphoma incidence ( J:125534 )

• unlike Sufu^GT(XB699)Byg heterozygotes, 8 of 55 mice develop lymphomas or thymomas likely due to Trp53^tm1Tyj

increased medulloblastoma incidence ( J:125534 )

• unlike Sufu^GT(XB699)Byg heterozygotes, 32 of 55 mice develop medulloblastomas that express TUBB3 and GFAP and exhibit increased apoptosis

nervous system

increased medulloblastoma incidence ( J:125534 )

• unlike Sufu^GT(XB699)Byg heterozygotes, 32 of 55 mice develop medulloblastomas that express TUBB3 and GFAP and exhibit increased apoptosis

muscle

increased rhabdomyosarcoma incidence ( J:125534 )

• unlike Sufu^GT(XB699)Byg heterozygotes, 5 of 55 mice develop rhabdomyosarcoma

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
medulloblastoma		DOID:0050902	OMIM:155255	J:173443

Genotype
MGI:6865653

cx107

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Vrk1^{Gt(RRR178)Byg}/Vrk1^{Gt(RRR178)Byg}
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

mortality/aging

decreased tumor-free survival time ( J:171525 )

• mice begin to succumb to tumors around 3 months of age, as seen in single Trp53^tm1Tyj homozygotes

early reproductive senescence ( J:171525 )

♂ • all three males tested produced one litter between 35 and 50 days postpartum (dpp), and two sired litters after 50 dpp (one at 68 dpp and one at 69 dpp); however, males become sterile after 69 dpp, similar to single Vrk1^{Gt(RRR178)Byg} homozygotes

neoplasm

increased tumor incidence ( J:171525 )

reproductive system

seminiferous tubule degeneration ( J:171525 )

♂ • marked loss/degeneration of the seminiferous tubular epithelium by 12 weeks of age

decreased testis weight ( J:171525 )

♂ • testis weight is significantly decreased at all ages examined between 6-8 and >12 weeks of age, similar to single Vrk1^{Gt(RRR178)Byg} homozygotes

early reproductive senescence ( J:171525 )

♂ • all three males tested produced one litter between 35 and 50 days postpartum (dpp), and two sired litters after 50 dpp (one at 68 dpp and one at 69 dpp); however, males become sterile after 69 dpp, similar to single Vrk1^{Gt(RRR178)Byg} homozygotes

abnormal spermatogenesis ( J:171525 )

♂ • progressive decline in spermatogenesis, starting at 8 weeks of age

♂ • loss of spermatogenesis occurs earlier than in single Vrk1^{Gt(RRR178)Byg} homozygotes

female infertility ( J:171525 )

♀ • females fail to produce litters or show any signs of pregnancy, similar to single Vrk1^{Gt(RRR178)Byg} female homozygotes

♀ • however, copulatory plugs are observed

male infertility ( J:171525 )

♂ • males fail to sire a litter after 69 days postpartum (dpp), despite continued presence of copulatory plugs

endocrine/exocrine glands

seminiferous tubule degeneration ( J:171525 )

♂ • marked loss/degeneration of the seminiferous tubular epithelium by 12 weeks of age

decreased testis weight ( J:171525 )

♂ • testis weight is significantly decreased at all ages examined between 6-8 and >12 weeks of age, similar to single Vrk1^{Gt(RRR178)Byg} homozygotes

Genotype
MGI:3840908

cx108

• Allelic Composition: Rev3l^tm1Ndew/Rev3l^tm1Ndew; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:75450 )

• mutant embryos are present up to 10.5 dpc in a near Mendelian ratio, but live embryos older than 11.5 dpc are not observed

embryo

abnormal embryonic tissue morphology ( J:75450 )

• abnormalities are seen in double mutant embryos beginning at 10.5 dpc, when apoptotic cells are detectable in the embryo proper

• similar to Rev3l homozygous embryos, by 10.5 dpc, double mutant embryos show growth retardation and a wide range of developmental dysmorphology, and considerable apoptotic cell death in the embryo proper compared to controls

Genotype
MGI:6191737

cx109

• Allelic Composition: Lyar^{Gt(RRG292)Byg}/Lyar^{Gt(RRG292)Byg}; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:263530 )

• the only two mice produced from breeding heterozygotes die by 8 months from thymic lymphoma

preweaning lethality, incomplete penetrance ( J:263530 )

• fewer than expected mice were recovered, motsly affecting female mice

nervous system

exencephaly ( J:263530 )

• in 11 of 18 mice at E16.5 to E18.5 mostly in female mice

neoplasm

increased T cell derived lymphoma incidence ( J:263530 )

• as in Trp53^tm1Tyj homozygotes

limbs/digits/tail

curly tail ( J:263530 )

• in some mice

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:263530 )

• as in Trp53^tm1Tyj homozygotes

Genotype
MGI:6191738

cx110

• Allelic Composition: Lyar^{Gt(RRG292)Byg}/Lyar⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

mortality/aging

preweaning lethality, incomplete penetrance ( J:263530 )

• fewer than expected mice were recovered

embryo

spina bifida ( J:263530 )

• in 1 of 27 mice

nervous system

spina bifida ( J:263530 )

• in 1 of 27 mice

exencephaly ( J:263530 )

• in 7 of 27 mice at E16.5 to E18.5 mostly in female mice

Genotype
MGI:5496437

cx111

• Allelic Composition: Trp53^tm1Tyj/?; Zfp148^Gt(XB878)Byg/Zfp148^Gt(XB878)Byg
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

mortality/aging

mortality/aging ( J:198319 )

N • deletion of 1 copy of Trp53 rescues Zfp148^Gt(XB878)Byg homozygotes from neonatal lethality

respiratory system

respiratory system phenotype ( J:198319 )

N • deletion of 1 or 2 copies of Trp53 rescues Zfp148^Gt(XB878)Byg homozygotes from proliferation arrest and lung defects such defective saccule development

Genotype
MGI:4943188

cx112

• Allelic Composition: Cd44^tm1Mak/Cd44^tm1Mak; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * C57BL/6J

neoplasm

decreased metastatic potential ( J:76201 )

• osteosarcoma on the lower back and on the skull, with significantly decreased metastasis

• incidence of ibrosarcomas, osteosarcomas, hemangiosarcomas, and histiocytic sarcomas, associated life span, and tumor weight on death are not affected

increased lymphoma incidence ( J:76201 )

• 17% have lymphoma, typical of those observed in Trp53^tm1Tyj/+ mice

• 23% have lymphomas, resembling anaplastic large cell lymphomas

• lymphoma is seen in conjunction with osteosarcoma, fibrosarcoma, and histiocytic sarcoma

Genotype
MGI:5554932

cx113

• Allelic Composition: Clp1^tm1.1Pngr/Clp1^tm1.1Pngr; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * C57BL/6J

mortality/aging

mortality/aging ( J:196364 )

N • complete rescue of neonatal lethality

neoplasm

increased tumor incidence ( J:196364 )

• as in Trp53^tm1Tyj homozygotes

nervous system

nervous system phenotype ( J:196364 )

N • mice exhibit normal diaphragm innervation and neuromuscular junction formation

muscle

muscle phenotype ( J:196364 )

N • young mice exhibit normal muscle strength

Genotype
MGI:5007743

cx114

• Allelic Composition: Cul9^tm1.2Yxi/Cul9^tm1.2Yxi; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * FVB/N

mortality/aging

mortality/aging ( J:170976 )

N • mice exhibit the same tumors-free survival time as Trp53^tm1Tyj homozygotes

neoplasm

neoplasm ( J:170976 )

N • mice exhibit the same tumors-free survival time as Trp53^tm1Tyj homozygotes

Genotype
MGI:5819195

cx115

• Allelic Composition: Cep63^{Gt(EUCE0251h11)Hmgu}/Cep63^{Gt(EUCE0251h11)Hmgu}; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6J

nervous system

nervous system phenotype ( J:224364 )

N • complete rescue of brain size and of cortical thickness, as determined in motor and visual cortex sections at P60

N • complete rescue of apoptosis in the cortex at E14.5, as shown by TUNEL staining

N • reduction of SOX2-positive neural progenitor cell (NPC) number is rescued; however, majority of the rescued NPCs are misplaced from the ventricular zone (extra-VZ)

Genotype
MGI:6286197

cx116

• Allelic Composition: Herc2^{Gt(AR0530)Wtsi}/Herc2^{Gt(AR0530)Wtsi}; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

mortality/aging

embryonic lethality, complete penetrance ( J:252045 )

• loss of Trp53 expression does not rescue the embryonic lethality of Herc2^{Gt(AR0530)Wtsi} homozygous mice

Genotype
MGI:5696984

cx117

• Allelic Composition: Sugt1^{Gt(RRS405)Byg}/Sugt1⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

increased tumor-free survival time ( J:226313 )

• significantly longer survival than of p53 knockout mice, but not as long as wild type controls

cellular

cellular phenotype ( J:226313 )

N • kinetochore formation, spindle checkpoint and ploidy are normal in MEFs

N • no significant difference in HRas-induced senescence and apoptosis between Sgt1+/ p53 MEF cells and Sgt1+/+ p53/ MEF cells

Genotype
MGI:2450866

cx118

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Tsg101^tm1Mak/Tsg101^tm1Mak
• Genetic Background: involves: 129P3/J * 129S2/SvPas * C57BL/6 * CD-1

mortality/aging

embryonic lethality, complete penetrance ( J:67553 )

• die between E8.5 and E10.5

embryo

decreased embryo size ( J:67553 )

• mutants are smaller than wild-type mice but larger than Tsg101^tm1Mak homozygous mutant mice at E8.5

growth/size/body

decreased embryo size ( J:67553 )

• mutants are smaller than wild-type mice but larger than Tsg101^tm1Mak homozygous mutant mice at E8.5

Genotype
MGI:4839757

cx119

• Allelic Composition: Emg1^tm1Hdin/Emg1^tm1Hdin; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S * 129S2/SvPas * 129X1/SvJ * CD-1 * ICR

embryo

abnormal preimplantation embryo development ( J:165972 )

embryonic growth arrest ( J:165972 )

• at the morula stage

absent blastocoele ( J:165972 )

Genotype
MGI:5554381

cx120

• Allelic Composition: Rasal2^{Gt(463C12)Cmhd}/Rasal2^{Gt(463C12)Cmhd}; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S * 129X1/SvJ * C57BL/6 * C57BL/6NCrl

mortality/aging

decreased tumor-free survival time ( J:202603 )

• mice typically die from the primary tumor, frequently lymphoma

neoplasm

increased colon adenoma incidence ( J:202603 )

• unlike in Trp53^tm1Tyj homozygotes

increased stomach tumor incidence ( J:202603 )

• unlike in Trp53^tm1Tyj homozygotes

increased mouth tumor incidence ( J:202603 )

• oral tumors unlike in Trp53^tm1Tyj homozygotes

increased liver tumor incidence ( J:202603 )

• unlike in Trp53^tm1Tyj homozygotes

increased hepatocellular carcinoma incidence ( J:202603 )

• unlike in Trp53^tm1Tyj homozygotes

increased metastatic potential ( J:202603 )

• highly metastatic mammary adenocarcinomas, hepatocellular carcinomas, lung adenocarcinomas and various sarcomas compared to in Trp53^tm1Tyj homozygotes

increased lymphoma incidence ( J:202603 )

• lymphomas resulting in death as in Trp53^tm1Tyj homozygotes

digestive/alimentary system

increased colon adenoma incidence ( J:202603 )

• unlike in Trp53^tm1Tyj homozygotes

increased stomach tumor incidence ( J:202603 )

• unlike in Trp53^tm1Tyj homozygotes

increased mouth tumor incidence ( J:202603 )

• oral tumors unlike in Trp53^tm1Tyj homozygotes

liver/biliary system

increased liver tumor incidence ( J:202603 )

• unlike in Trp53^tm1Tyj homozygotes

increased hepatocellular carcinoma incidence ( J:202603 )

• unlike in Trp53^tm1Tyj homozygotes

Genotype
MGI:5554383

cx121

• Allelic Composition: Rasal2^{Gt(463C12)Cmhd}/Rasal2⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S * 129X1/SvJ * C57BL/6 * C57BL/6NCrl

neoplasm

increased metastatic potential ( J:202603 )

• highly metastatic mammary adenocarcinomas, hepatocellular carcinomas, lung adenocarcinomas and various sarcomas compared to in Trp53^tm1Tyj homozygotes

Genotype
MGI:2675374

cx122

• Allelic Composition: Bard1^tm1Thl/Bard1^tm1Thl; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:84329 )

• survived through E9.5

cellular

chromosome breakage ( J:84329 )

• 44% of mitotic spreads showed abnormal chromosome number, usually reduced

embryo

decreased embryo size ( J:84329 )

• developmentally retarded by E9.5

open neural tube ( J:84329 )

• seen at E9.5

growth/size/body

decreased embryo size ( J:84329 )

• developmentally retarded by E9.5

nervous system

open neural tube ( J:84329 )

• seen at E9.5

Genotype
MGI:5559534

cx123

• Allelic Composition: Rtel1^tm2.1Hdin/Rtel1^tm2.1Hdin; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6

mortality/aging

premature death ( J:202812 )

• compared with Rtel1^tm2.1Hdin/Rtel1⁺ Trp53^tm1Tyj/Trp53^tm1Tyj mice

neoplasm

increased lymphoma incidence ( J:202812 )

• as in Trp53^tm1Tyj homozygotes

increased medulloblastoma incidence ( J:202812 )

• unlike in Trp53^tm1Tyj homozygotes

increased sarcoma incidence ( J:202812 )

• as in Trp53^tm1Tyj homozygotes

increased teratoma incidence ( J:202812 )

• as in Trp53^tm1Tyj homozygotes

decreased tumor latency ( J:202812 )

• tumor formation occurs within 115+/-31 days compared with 147+/-35 days for Rtel1^tm2.1Hdin/Rtel1⁺ Trp53^tm1Tyj/ Trp53^tm1Tyj mice

cellular

abnormal telomere morphology ( J:202812 )

• extensive sister chromatid fusions, end-to-end fusions with telomeric repeats and fragile telomeres in tumor cells unlike in tumor cells from Trp53^tm1Tyj homozygotes

nervous system

increased medulloblastoma incidence ( J:202812 )

• unlike in Trp53^tm1Tyj homozygotes

Genotype
MGI:3814378

cx124

• Allelic Composition: Kat5^tm1Jwl/Kat5⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6

neoplasm

increased tumor incidence ( J:125164 )

• mice exhibit the same disease progression as in Trp53^tm1Tyj homozygotes

Genotype
MGI:3690370

cx125

• Allelic Composition: Ptch1^tm1Mps/Ptch1⁺; Ptch2^tm1Pmc/Ptch2⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6

neoplasm

neoplasm ( J:112118 )

N • mice show no increase in tumor incidence compared to Ptch1/Trp53 double null mice

Genotype
MGI:3690369

cx126

• Allelic Composition: Ptch2^tm1Pmc/Ptch2^tm1Pmc; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * C57BL/6

neoplasm

neoplasm ( J:112118 )

N • double mutants show similar tumor profile and latency as Trp53-null animals (11/20 develop thymoma and/or sarcoma by 4 months of age)

Genotype
MGI:3655347

cx127

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺; Xrcc2^tm1Pmc/Xrcc2^tm1Pmc
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * C57BL/6

growth/size/body

decreased body weight ( J:111068 )

• mice are smaller and less robust than wild-type littermates

neoplasm

increased T cell derived lymphoma incidence ( J:111068 )

• thymoma is detected

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:111068 )

• thymoma is detected

Genotype
MGI:3710321

cx128

• Allelic Composition: Cdkn2c^tm1Bbd/Cdkn2c^tm1Bbd; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * C57BL/6

nervous system

abnormal neuron differentiation ( J:102702 )

• lack of Cdkn2c results in earler evidence of tumor formation, shown by increased neuronal proliferation in cerebellum molecular layer, compared to Cdkn2c-sufficient mice mutants

• in 1-month old mutants injected in the cerebella with BrdU, analysis 9 hours post-injection shows proliferating cells in the superficial molecular layer and the internal granule layer while proliferation has ceased in wild-type cerebella

• there is 3-fold increase in proliferating cells relative to control cerebella

• 50% of double null granule neuronal precursor cells (GNPs) from P12 mice show proliferative capacity compared to wild-type cells (in absence of Shh in culture medium); wild-type cells from P7 mice have mostly exited the cell cycle after 3 days in culture, while many double-null cells continue to incorporate BrdU

• in culture, labeled wild-type cells from P10 and 12 mice that are exposed to Shh show greatly reduced BrdU incorporation compared to double-null cells after 72 hours

increased medulloblastoma incidence ( J:102702 )

• 18/24 (75%) of animals receiving 4 Gy radiation at P5 or 6 develop cerebellar tumors

neoplasm

increased medulloblastoma incidence ( J:102702 )

• 18/24 (75%) of animals receiving 4 Gy radiation at P5 or 6 develop cerebellar tumors

cellular

abnormal neuron differentiation ( J:102702 )

• lack of Cdkn2c results in earler evidence of tumor formation, shown by increased neuronal proliferation in cerebellum molecular layer, compared to Cdkn2c-sufficient mice mutants

• in 1-month old mutants injected in the cerebella with BrdU, analysis 9 hours post-injection shows proliferating cells in the superficial molecular layer and the internal granule layer while proliferation has ceased in wild-type cerebella

• there is 3-fold increase in proliferating cells relative to control cerebella

• 50% of double null granule neuronal precursor cells (GNPs) from P12 mice show proliferative capacity compared to wild-type cells (in absence of Shh in culture medium); wild-type cells from P7 mice have mostly exited the cell cycle after 3 days in culture, while many double-null cells continue to incorporate BrdU

• in culture, labeled wild-type cells from P10 and 12 mice that are exposed to Shh show greatly reduced BrdU incorporation compared to double-null cells after 72 hours

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
medulloblastoma		DOID:0050902	OMIM:155255	J:102702

Genotype
MGI:3710320

cx129

• Allelic Composition: Cdkn2c^tm1Bbd/Cdkn2c⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * C57BL/6

neoplasm

increased medulloblastoma incidence ( J:102702 )

• 15/17 (88%) of animals receiving 4 Gy radiation at P5 or 6 develop cerebellar tumors

nervous system

increased medulloblastoma incidence ( J:102702 )

• 15/17 (88%) of animals receiving 4 Gy radiation at P5 or 6 develop cerebellar tumors

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
medulloblastoma		DOID:0050902	OMIM:155255	J:102702

Genotype
MGI:3710319

cx130

• Allelic Composition: Cdkn2c^tm1Bbd/Cdkn2c⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * C57BL/6

neoplasm

increased medulloblastoma incidence ( J:102702 )

• small increase in tumor incidence (2/20) after irradiation at P5 or 6 with 4 Gy radiation

nervous system

increased medulloblastoma incidence ( J:102702 )

• small increase in tumor incidence (2/20) after irradiation at P5 or 6 with 4 Gy radiation

Genotype
MGI:3655298

cx131

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Xrcc2^tm1Pmc/Xrcc2^tm1Pmc
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * C57BL/6

mortality/aging

perinatal lethality, incomplete penetrance ( J:111068 )

• mice are less robust than Lig4/Trp53 double homozygotes and often die perinatally of indeterminate causes

growth/size/body

decreased body weight ( J:111068 )

• mice are smaller and less robust than wild-type littermates

nervous system

decreased neuron apoptosis ( J:111068 )

• apoptosis is markedly reduced in double mutants

increased medulloblastoma incidence ( J:111068 )

neoplasm

increased tumor incidence ( J:111068 )

• surviving double mutants all develop multiple tumor types with a rapid onset and with different tumor types present by 10 weeks of age

increased skin tumor incidence ( J:111068 )

increased lymphoma incidence ( J:111068 )

• these are B220 negative and distinct from the pro-B cell lymphomas

increased T cell derived lymphoma incidence ( J:111068 )

• thymomas contain multiple chromosomal rearrangements but no recurring chromosomal rearrangements are observed in primary tumors

increased medulloblastoma incidence ( J:111068 )

increased sarcoma incidence ( J:111068 )

integument

increased skin tumor incidence ( J:111068 )

cellular

decreased neuron apoptosis ( J:111068 )

• apoptosis is markedly reduced in double mutants

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:111068 )

• thymomas contain multiple chromosomal rearrangements but no recurring chromosomal rearrangements are observed in primary tumors

Genotype
MGI:5509171

cx132

• Allelic Composition: Prmt6^tm1.2Rchd/Prmt6^tm1.2Rchd; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J * FVB/N

cellular

cellular phenotype ( J:199753 )

N • mouse embryonic fibroblasts exhibit normal senescence

Genotype
MGI:2677843

cx133

• Allelic Composition: Terf1^tm1Tdl/Terf1^tm1Tdl; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas

mortality/aging

prenatal lethality, complete penetrance ( J:85440 )

• no homozygotes were born

• timing of lethality was somewhat attenuated

• undersized surviving embryos found at E7-7.5

• 2 surviving embryos at E8-8.5

embryo

disorganized extraembryonic tissue ( J:85440 )

• extraembryonic structures generally disorganized

Genotype
MGI:3776067

cx134

• Allelic Composition: Nf1^tm1Tyj/Nf1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas

nervous system

nervous system phenotype ( J:131914 )

N • neural crest stem cells do not abnormally persist in the peripheral nervous system in adult mice

increased neurofibrosarcoma incidence ( J:131914 )

• form by 6 months of age

neoplasm

increased neurofibrosarcoma incidence ( J:131914 )

• form by 6 months of age

Genotype
MGI:3819978

cx135

• Allelic Composition: Ccnd3^tm1Pisc/Ccnd3^tm1Pisc; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas

mortality/aging

premature death ( J:88120 )

• animals die by about 26 weeks

neoplasm

increased T cell derived lymphoma incidence ( J:88120 )

• mice develop T cell malignancies with similar kinetics as Trp53-null mice

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:88120 )

• mice develop T cell malignancies with similar kinetics as Trp53-null mice

Genotype
MGI:3850680

cx136

• Allelic Composition: Mdm4^tm1Glo/Mdm4^tm1Glo; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas

mortality/aging

mortality/aging ( J:71532 , J:93838 )

N • mice are born in expected Mendelian ratios (J:71532)

N • mice are born in expected Mendelian ratios (J:93838)

Genotype
MGI:3850686

cx137

• Allelic Composition: Mdm4^tm1Glo/Mdm4^tm1Glo; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas

mortality/aging

preweaning lethality, complete penetrance ( J:93838 )

• no mice are present at 3 weeks of age

embryo

abnormal embryo development ( J:93838 )

• embryos are abnormal at E9.5

Genotype
MGI:4355022

cx138

• Allelic Composition: Atr^tm1Ofc/Atr^tm1Ofc; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas

mortality/aging

premature death ( J:151542 )

• mice do not survive beyond 2 months

prenatal lethality, incomplete penetrance ( J:151542 )

• few mice are born

premature aging ( J:151542 )

• mice exhibit a more severe premature aging syndrome than in Atr^tm1Ofc homozygotes

skeleton

micrognathia ( J:151542 )

kyphosis ( J:151542 )

osteoporosis ( J:151542 )

growth/size/body

decreased body weight ( J:151542 )

small thoracic cavity ( J:151542 )

microcephaly ( J:151542 )

proportional dwarf ( J:151542 )

• more severe than in Atr^tm1Ofc homozygotes

cellular

increased embryonic tissue cell apoptosis ( J:151542 )

• apoptosis in the whole embryos is greater than in Atr^tm1Ofc homozygotes

abnormal DNA replication ( J:151542 )

• embryos exhibit replicative stress-initiated DNA damage response unlike wild-type mice

homeostasis/metabolism

abnormal DNA replication ( J:151542 )

• embryos exhibit replicative stress-initiated DNA damage response unlike wild-type mice

craniofacial

micrognathia ( J:151542 )

hematopoietic system

pancytopenia ( J:151542 )

embryo

increased embryonic tissue cell apoptosis ( J:151542 )

• apoptosis in the whole embryos is greater than in Atr^tm1Ofc homozygotes

Genotype
MGI:4420470

cx139

• Allelic Composition: Rb1^tm1Tyj/Rb1^tm1Tyj; Tg(Rb1)1Blg/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas

mortality/aging

postnatal lethality ( J:65679 )

• fewer than expected mice are obtained (no time point of death given)

muscle

abnormal skeletal muscle fiber morphology ( J:65679 )

• skeletal muscle fibers are no different than in Rb1^tm1Tyj/Rb1^tm1Tyj Tg(Rb1)1Blg mice

abnormal muscle physiology ( J:65679 )

• at E18.5, skeletal muscle exhibit an increase in apoptosis compared with Rb1^tm1Tyj/Rb1⁺ Tg(Rb1)1Blg mice

behavior/neurological

hyporesponsive to tactile stimuli ( J:65679 )

hunched posture ( J:65679 )

cellular

polyploidy ( J:65679 )

• as in Rb1^tm1Tyj/Rb1^tm1Tyj Tg(Rb1)1Blg mice

abnormal cell cycle ( J:65679 )

• as in Rb1^tm1Tyj/Rb1^tm1Tyj Tg(Rb1)1Blg mice, myotubes are unable to exhibit the cell cycle and accumulate enlarged nuclei unlike wild-type myotubes

abnormal retina apoptosis ( J:65679 )

• lens apoptosis is reduced 10-fold compared to in Rb1^tm1Tyj/Rb1^tm1Tyj Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Rb1)1Blg mice

vision/eye

abnormal retina apoptosis ( J:65679 )

• lens apoptosis is reduced 10-fold compared to in Rb1^tm1Tyj/Rb1^tm1Tyj Trp53^tm1Tyj/Trp53^tm1Tyj Tg(Rb1)1Blg mice

Genotype
MGI:6780002

cx140

• Allelic Composition: Nbn^em3Jpt/Nbn^em3Jpt; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas

muscle

increased leiomyosarcoma incidence ( J:251434 )

increased rhabdomyosarcoma incidence ( J:251434 )

neoplasm

increased leiomyosarcoma incidence ( J:251434 )

increased rhabdomyosarcoma incidence ( J:251434 )

increased histiocytic sarcoma incidence ( J:251434 )

increased squamous cell carcinoma incidence ( J:251434 )

increased hemangiosarcoma incidence ( J:251434 )

decreased tumor latency ( J:251434 )

• mice exhibit a reduced latency of tumor development, with a mean tumor-free survival decreased by 27-50 days relative to single Trp53 homozygous mice

Genotype
MGI:6780003

cx141

• Allelic Composition: Nbn^em4Jpt/Nbn^em4Jpt; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas

neoplasm

increased leiomyosarcoma incidence ( J:251434 )

increased rhabdomyosarcoma incidence ( J:251434 )

increased histiocytic sarcoma incidence ( J:251434 )

increased squamous cell carcinoma incidence ( J:251434 )

increased hemangiosarcoma incidence ( J:251434 )

decreased tumor latency ( J:251434 )

• mice exhibit a reduced latency of tumor development, with a mean tumor-free survival decreased by 27-50 days relative to single Trp53 homozygous mice

muscle

increased leiomyosarcoma incidence ( J:251434 )

increased rhabdomyosarcoma incidence ( J:251434 )

Genotype
MGI:3702081

cx142

• Allelic Composition: Gnl3^{Gt(W223E05)Wrst}/Gnl3^{Gt(W223E05)Wrst}; Trp53^tm1Tyj/Trp53^tm5Tyj
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:118144 )

• loss of Trp53 expression does not alter or delay the lethality

embryo

embryonic growth arrest ( J:118144 )

• loss of Trp53 expression does not alter or delay the overall phenotype

cellular

decreased cell proliferation ( J:118144 )

• loss of Trp53 expression does not alter or delay the impairment of cell proliferation

Genotype
MGI:5289961

cx143

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺; Trp63^tm1Fmc/Trp63⁺
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:98958 )

• median age of survival is 7 months

premature aging ( J:98958 )

• 40% of mutants exhibit increased signs of aging, developing severe degenerative disc disease of the spine between 6 and 18 months of age

neoplasm

increased metastatic potential ( J:98958 )

• about 50% of mutants develop metastatic tumors

increased tumor incidence ( J:98958 )

• mutants exhibit an increase in tumor burden compared to heterozygous Trp53 mice, with 90% of mutant mice having multiple tumors of the same or distinct types compared to only 10% in Trp53 heterozygotes

• mutants develop collision tumors composed of mammary adenocarcinomas directly adjacent to squamous cell carcinomas and/or rhabdomyosarcomas

• tumors exhibit loss of heterozygosity of one or both genes

increased mammary adenocarcinoma incidence ( J:98958 )

• 10% of mutants develop mammary adenocarcinomas

increased T cell derived lymphoma incidence ( J:98958 )

• 10% of mutants develop thymic lymphomas

increased rhabdomyosarcoma incidence ( J:98958 )

• 20% of mutants develop rhabdomyosarcomas

increased chronic myelocytic leukemia incidence ( J:98958 )

• 15% of mutants develop myelogenous leukemia

increased squamous cell carcinoma incidence ( J:98958 )

• 50% of mutants develop squamous cell carcinomas in multiple tissues (larynx, pharynx, cervix, and esophagus)

increased urinary bladder transitional cell carcinoma incidence ( J:98958 )

• 20% of mutants develop transitional cell carcinoma of the bladder

increased osteosarcoma incidence ( J:98958 )

• 20% of mutants develop osteosarcomas

skeleton

increased osteosarcoma incidence ( J:98958 )

• 20% of mutants develop osteosarcomas

intervertebral disk degeneration ( J:98958 )

• 40% of mutants develop severe degenerative disc disease of the spine between 6 and 18 months of age

• degenerative disc disease is consistent with spondylosis and is most frequent in the cervical and thoracic region

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:98958 )

• 10% of mutants develop mammary adenocarcinomas

increased T cell derived lymphoma incidence ( J:98958 )

• 10% of mutants develop thymic lymphomas

integument

increased mammary adenocarcinoma incidence ( J:98958 )

• 10% of mutants develop mammary adenocarcinomas

muscle

increased rhabdomyosarcoma incidence ( J:98958 )

• 20% of mutants develop rhabdomyosarcomas

renal/urinary system

increased urinary bladder transitional cell carcinoma incidence ( J:98958 )

• 20% of mutants develop transitional cell carcinoma of the bladder

Genotype
MGI:3620760

cx144

• Allelic Composition: Rr149356^tm1Che/Rr149356^tm1Che; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * C57BL/6

immune system

abnormal double-negative T cell morphology ( J:106246 )

• 24% of double negative thymocytes are apoptotic

abnormal double-positive T cell morphology ( J:106246 )

• 36% of double positive thymocytes are apoptotic

• double positive cells start losing CD4 expression around 7 weeks to become CD8 single positive

neoplasm

increased T cell derived lymphoma incidence ( J:106246 )

• 2/3 of mice develop thymic lymphomas

• single positive Cd8 cells are immature and abnormal, make up 60% of thymocytes by 8 weeks

• large terminal lymphomas present by 11-17 weeks of age

• mean survival of 14 weeks

decreased metastatic potential ( J:106246 )

• inefficient metastasis

hematopoietic system

abnormal double-negative T cell morphology ( J:106246 )

• 24% of double negative thymocytes are apoptotic

abnormal double-positive T cell morphology ( J:106246 )

• 36% of double positive thymocytes are apoptotic

• double positive cells start losing CD4 expression around 7 weeks to become CD8 single positive

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:106246 )

• 2/3 of mice develop thymic lymphomas

• single positive Cd8 cells are immature and abnormal, make up 60% of thymocytes by 8 weeks

• large terminal lymphomas present by 11-17 weeks of age

• mean survival of 14 weeks

Genotype
MGI:5289964

cx145

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺; Trp73^tm1Fmc/Trp73⁺
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:98958 )

• median age of survival is 6 months

neoplasm

increased metastatic potential ( J:98958 )

• about 45% of mutants develop metastatic tumors

increased tumor incidence ( J:98958 )

• mutants exhibit an increase in tumor burden compared to heterozygous Trp53 mice, with 75% of mutant mice having multiple tumors of the same or distinct types compared to only 10% in Trp53 heterozygotes

• tumors exhibit loss of heterozygosity of one or both genes

increased pancreatic acinar cell carcinoma incidence ( J:98958 )

• 15% of mutants develop acinar pancreatic carcinoma

increased T cell derived lymphoma incidence ( J:98958 )

• 22.5% of mutants develop thymic lymphomas

increased hepatocellular carcinoma incidence ( J:98958 )

• 15% of mutants develop hepatocellular carcinomas

increased lung adenocarcinoma incidence ( J:98958 )

• 10% of mutants develop lung adenocarcinomas

increased sarcoma incidence ( J:98958 )

• 50% of mutants develop sarcomas

endocrine/exocrine glands

increased pancreatic acinar cell carcinoma incidence ( J:98958 )

• 15% of mutants develop acinar pancreatic carcinoma

increased T cell derived lymphoma incidence ( J:98958 )

• 22.5% of mutants develop thymic lymphomas

respiratory system

increased lung adenocarcinoma incidence ( J:98958 )

• 10% of mutants develop lung adenocarcinomas

liver/biliary system

increased hepatocellular carcinoma incidence ( J:98958 )

• 15% of mutants develop hepatocellular carcinomas

Genotype
MGI:3587059

cx146

• Allelic Composition: Nf1^tm1Tyj/?; Trp53^tm1Tyj/?; Mastr^129S4/SvJae/?
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J

neoplasm

decreased tumor incidence ( J:92444 )

• astrocytoma resistance

Genotype
MGI:3587060

cx147

• Allelic Composition: Nf1^tm1Tyj/?; Trp53^tm1Tyj/?; Mastr^C57BL/6J/?
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J

neoplasm

increased astrocytoma incidence ( J:92444 )

• astrocytoma susceptibility

nervous system

increased astrocytoma incidence ( J:92444 )

• astrocytoma susceptibility

Genotype
MGI:3623223

cx148

• Allelic Composition: Rad51b^tm1Kmic/Rad51b^tm1Kmic; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J

mortality/aging

embryonic lethality between somite formation and embryo turning ( J:58601 )

• embryonic development progress further than Rad51l1^tm1Kmic homozygous embryo

Genotype
MGI:6502662

cx149

• Allelic Composition: Map9^tm1.2Bcgen/Map9^tm1.2Bcgen; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJaeSor * BALB/cJ * C57BL/6

cellular

aneuploidy ( J:299895 )

• aneuploidy frequency in splenocytes is higher (58%) compared to single Map9 heterozygotes (39%) or single p53 heterozygotes (23%) or wild-type mice (17%)

Genotype
MGI:3616708

cx150

• Allelic Composition: Mdm4^tm2.1Glo/Mdm4^tm2.1Glo; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6J

normal phenotype

no abnormal phenotype detected ( J:104114 )

• double homozygotes are viable and born at the expected ratio, exhibiting rescue of the embryonic lethality of single homozygous Mdm4 mice, however no further phenotypic analysis is reported

Genotype
MGI:3700235

cx151

• Allelic Composition: Mdm4^{Gt(VICTR20)7Lex}/Mdm4^{Gt(VICTR20)7Lex}; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S5/SvEvBrd

mortality/aging

mortality/aging ( J:77907 )

N • double homozygotes are viable, unlike mice homozygous for the Mdm4 allele alone

embryo

embryo phenotype ( J:77907 )

N • appear indistinguishable from control littermates at E10.5, unlike mice homozygous for the Mdm4 mutation alone

cellular

abnormal cell cycle checkpoint function ( J:77907 )

• gamma-irradiation fails to produce an increase in the relative number of cells in G1 compared to S phase similar to what is seen in MEFs homozygous for the Trp53 allele alone

decreased cellular sensitivity to ultraviolet irradiation ( J:77907 )

• reduced sensitivity to UV-induced cell death in MEFs similar to cells homozygous for Trp53 alone

increased fibroblast proliferation ( J:77907 )

• similar to MEFs homozygous for the Trp53 allele alone, proliferation is increased relative to control cells

Genotype
MGI:5568932

cx152

• Allelic Composition: Pip4k2b^{Gt(Betageo)1Lca}/Pip4k2b^{Gt(Betageo)1Lca}; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S5/SvEvBrd

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:205288 )

• lethality by E12.5

embryo

open neural tube ( J:205288 )

• failure of neural tube closure

nervous system

open neural tube ( J:205288 )

• failure of neural tube closure

exencephaly ( J:205288 )

Genotype
MGI:3700236

cx153

• Allelic Composition: Mdm4^{Gt(VICTR20)7Lex}/Mdm4^{Gt(VICTR20)7Lex}; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S5/SvEvBrd

mortality/aging

preweaning lethality, complete penetrance ( J:77907 )

• no viable mice are found, no specific time of death is provided

embryo

decreased embryo size ( J:77907 )

• reduced in size compared to double heterozygous controls; however, this reduction is slight compared to mice homozygous for the Mdm4 mutation alone

growth/size/body

decreased embryo size ( J:77907 )

• reduced in size compared to double heterozygous controls; however, this reduction is slight compared to mice homozygous for the Mdm4 mutation alone

Genotype
MGI:3608498

cx154

• Allelic Composition: Npm1^{Gt(VICTR37)704Lex}/Npm1^{Gt(VICTR37)704Lex}; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S5/SvEvBrd * C57BL/6

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:101353 )

• embryos are found up to E12.5 and these are larger than Npm1^{Gt(VICTR37)1Lex} homozygous embryos indicating a diminished severity in phenotype

cellular

abnormal apoptosis ( J:101353 )

• diminished caspase 3 positive cells in embryos relative to Npm1^{Gt(VICTR37)1Lex} homozygotes

increased fibroblast proliferation ( J:101353 )

• BrdU staining of embryos shows approximately 35% increase in fibroblasts of double homozygotes relative to Trp53^tm1Tyj homozygotes

• explanted fibroblasts show unlimited growth potential distinct from the arrested growth of Npm1^{Gt(VICTR37)1Lex} homozygotes

Genotype
MGI:5002826

cx155

• Allelic Composition: Rag1^tm1Fwa/Rag1^tm1Fwa; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac

cellular

cellular phenotype ( J:170462 )

N • no genomic instability is observed

Genotype
MGI:6357935

cx156

• Allelic Composition: Set^tm1.1Wgu/Set^tm1.1Wgu; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac

mortality/aging

prenatal lethality, complete penetrance ( J:276962 )

• while no viable double homozygous mice are seen at birth, viable and morphologically normal double homozygous mice are found at E11.5 and E13.5 indicating a delay in lethality compared to mice homozygous for Set^tm1.1Wgu alone

Genotype
MGI:3840834

cx157

• Allelic Composition: Rag1^tm1Jsek/Rag1^tm1Jsek; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac

mortality/aging

decreased survivor rate ( J:146912 )

• mice have significantly decreased survival compared to Trp53^tm1Tyj homozygote controls

premature death ( J:146912 )

• all mice die from lymphomas by 30 weeks of age

neoplasm

increased T cell derived lymphoma incidence ( J:146912 )

• 90% of lymphomas in these mice are immature TCRbeta^- T cell lymphomas

• thymic lymphomas feature frequent clonal translocations and fusions that are karyotypically distinct from lymphomas isolated from Trp53^tm1Tyj homozygotes

cellular

spontaneous chromosome breakage ( J:146912 )

• 6 of 7 lymphomas contain chromosomal translocations and/or short-arm fusions in a clonal population of tumor cells

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:146912 )

• 90% of lymphomas in these mice are immature TCRbeta^- T cell lymphomas

• thymic lymphomas feature frequent clonal translocations and fusions that are karyotypically distinct from lymphomas isolated from Trp53^tm1Tyj homozygotes

Genotype
MGI:5002824

cx158

• Allelic Composition: Rag2^tm1.1Mss/Rag2^tm1.1Mss; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac

mortality/aging

premature death ( J:170462 )

• 100% of mice die within 16 weeks with aggressive lymphomas

neoplasm

increased lymphoma incidence ( J:170462 )

• 100% of mice die within 16 weeks with aggressive lymphomas

increased T cell derived lymphoma incidence ( J:170462 )

• tumor cells are highly proliferative

• tumor cells express CD4+ and CD8+ but little surface TCR

• tumors are detected at 4-6 weeks in the thymus but not in other organs

• cytogenetic aberrations in tumor cells

cellular

abnormal chromosome morphology ( J:170462 )

• chromosome breaks and fusions in tumor cells

• recurrent translocations on Chromosomes 14 and 16 where TCR genes are located and on Chromosomes 12, 6, and 16 where Ig genes are located

• translocations involve Chromosomes 12 and 14 in particular

aneuploidy ( J:170462 )

• observed in tumor cells

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:170462 )

• tumor cells are highly proliferative

• tumor cells express CD4+ and CD8+ but little surface TCR

• tumors are detected at 4-6 weeks in the thymus but not in other organs

• cytogenetic aberrations in tumor cells

Genotype
MGI:2450431

cx159

• Allelic Composition: Rad50^tm2Jpt/Rad50^tm2Jpt; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6

mortality/aging

premature death ( J:78820 )

• mean age of death is 4.5 months

neoplasm

increased T cell derived lymphoma incidence ( J:78820 )

immune system

immune system phenotype ( J:78820 )

N • B cell numbers increased 5-20 fold compared to Rad50^tm2Jpt homozygous mice

reproductive system

abnormal testis morphology ( J:78820 )

♂ • suppression of testicular apoptosis

♂ • normal meiotic progression

endocrine/exocrine glands

abnormal testis morphology ( J:78820 )

♂ • suppression of testicular apoptosis

♂ • normal meiotic progression

increased T cell derived lymphoma incidence ( J:78820 )

Genotype
MGI:3850704

cx160

• Allelic Composition: Mdm2^tm1Glo/Mdm2⁺; Mdm4^tm1Glo/Mdm4⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6

mortality/aging

mortality/aging ( J:123661 )

N • mice are born in expected Mendelian ratios

Genotype
MGI:3850702

cx161

• Allelic Composition: Mdm2^tm1Glo/Mdm2⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6

mortality/aging

mortality/aging ( J:123661 )

N • mice exhibit normal mortality in response to treatment with ionizing radiation

Genotype
MGI:3618360

cx162

• Allelic Composition: Bhlha15^tm2(Kras)Skz/Bhlha15⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6

mortality/aging

premature death ( J:105076 )

• mutants have a median survival of 6.5 months compared to median survival of 10.8 months and 11.7 months of each single heterozygote respectively

neoplasm

increased hepatocellular carcinoma incidence ( J:105076 )

• double heterzygotes show fewer tumors of this type compared with the single heterozygotes

increased metastatic potential ( J:105076 )

• doubly heterozygous mice show an increase in metastatic disease compared to single heterozygotes

liver/biliary system

increased hepatocellular carcinoma incidence ( J:105076 )

• double heterzygotes show fewer tumors of this type compared with the single heterozygotes

Genotype
MGI:3762617

cx163

• Allelic Composition: Arhgap1^tm1Yizh/Arhgap1^tm1Yizh; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6

cellular

cellular phenotype ( J:119516 )

N • MEFs grow at a rate between that of heterozygous Trp53 MEFs and wild-type cells, indicating that the senescence seen in homozygous Arhgap1 mutant MEFs is rescued

Genotype
MGI:3850700

cx164

• Allelic Composition: Mdm4^tm1Glo/Mdm4⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6

mortality/aging

mortality/aging ( J:123661 )

N • mice exhibit normal mortality in response to treatment with ionizing radiation

Genotype
MGI:3702291

cx165

• Allelic Composition: Hus1^tm1Led/Hus1^tm2Rsw; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6

neoplasm

neoplasm ( J:118898 )

N • mice do not show differences in tumor development compared to wild-type Hus1, Trp53 heterozygotes

Genotype
MGI:3663892

cx166

• Allelic Composition: Metap2^tm1.2Ccr/Metap2^tm1.2Ccr; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * FVB/N

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:111701 )

• develop past gastrulation and survive until E9.5

embryo

embryo tissue necrosis ( J:111701 )

• embryos become necrotic around E9.5

decreased embryo size ( J:111701 )

• 6 of 7 E9.5 embryos are smaller than controls but show developed anterior-posterior patterning with head, trunk, and tail region

growth/size/body

decreased embryo size ( J:111701 )

• 6 of 7 E9.5 embryos are smaller than controls but show developed anterior-posterior patterning with head, trunk, and tail region

cardiovascular system

abnormal vascular development ( J:111701 )

• embryos form an initial vascular network, especially in the brain, however it is less complex than in controls

cellular

embryo tissue necrosis ( J:111701 )

• embryos become necrotic around E9.5

Genotype
MGI:3629206

cx167

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺; Trp53bp2^tm1Xlu/Trp53bp2^tm1Xlu
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J

mortality/aging

prenatal lethality, incomplete penetrance ( J:108701 )

• only 20% of the expected number of pups are found at birth

Genotype
MGI:3629205

cx168

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Trp53bp2^tm1Xlu/Trp53bp2^tm1Xlu
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:108701 )

• no homozygous offspring are found in timed matings from E11.5-17.5

Genotype
MGI:3629207

cx169

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺; Trp53bp2^tm1Xlu/Trp53bp2⁺
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J

neoplasm

increased tumor incidence ( J:108701 )

• 26% of double heterozygotes develop tumors over a 72 week period

increased lymphoma incidence ( J:108701 )

• lymphoma development is accelerated in compared to Trp53 heterozygotes with wild-type Trp53bp2; at 42 weeks there is a significant difference in the onset between the two genotypes

• at 72 weeks the difference in onset of lymphoma development is not significant

Genotype
MGI:5140356

cx170

• Allelic Composition: Rpl27a^Sfa/Rpl27a⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J

mortality/aging

increased tumor-free survival time ( J:174216 )

• prolonged survival compared to mice heterozygous for the Trp53 allele alone

neoplasm

increased metastatic potential ( J:174216 )

• compared to mice heterozygous for the Trp53 allele alone

abnormal tumor incidence ( J:174216 )

• increase in tumor type multiplicity compared to mice heterozygous for the Trp53 allele alone

decreased lymphoma incidence ( J:174216 )

• compared to mice heterozygous for the Trp53 allele alone

increased tumor latency ( J:174216 )

• tumors appear at about 13 months of age compared to about 9 months of age in mice heterozygous for the Trp53 allele alone

Genotype
MGI:3850689

cx171

• Allelic Composition: Mdm2^tm1Glo/Mdm2^tm1Glo; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd

mortality/aging

mortality/aging ( J:93838 )

N • mice are born in expected Mendelian ratios

Genotype
MGI:4941811

cx172

• Allelic Composition: Dclre1a^tm1Rleg/Dclre1a^tm1Rleg; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd

mortality/aging

premature death ( J:102381 )

• significant decrease in the survival of double homozygous mice compared to control littermates

• time to 50% survival was approximately 4 months for the double homozygous mice compared to 5.5 months for the Trp53 homozygous mice

neoplasm

increased lymphoma incidence ( J:102381 )

• a majority of double homozygous animals developed nonthymic lymphomas

increased T cell derived lymphoma incidence ( J:102381 )

• 100% of the double homozygous mice developed thymic lymphomas

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:102381 )

• 100% of the double homozygous mice developed thymic lymphomas

Genotype
MGI:4941812

cx173

• Allelic Composition: Dclre1a^tm1Rleg/Dclre1a⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd

neoplasm

increased sarcoma incidence ( J:102381 )

• sarcomas were observed

Genotype
MGI:3615887

cx174

• Allelic Composition: Nbn^tm1Jpt/Nbn^tm1Jpt; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd

mortality/aging

premature death ( J:75956 )

• die by 4 months of age

neoplasm

increased lymphoma incidence ( J:75956 )

increased teratoma incidence ( J:75956 )

decreased tumor latency ( J:75956 )

• tumors arise significantly earlier than in single homozygous Trp53 mice, although tumor spectrum is no different than that of homozygous Trp53 mice

Genotype
MGI:3850688

cx175

• Allelic Composition: Mdm2^tm1Glo/Mdm2^tm1Glo; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd

embryo

abnormal embryonic tissue morphology ( J:93838 )

• no embryos are found at E8.5

Genotype
MGI:3690106

cx176

• Allelic Composition: Pot1a^tm1Schg/Pot1a^tm1.1Schg; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6

cellular

cellular phenotype ( J:112184 )

N • in double null MEFs, senescence-like growth arrest is not observed like in p53-intact, Pot1a-null MEFs

abnormal chromosome morphology ( J:112184 )

• extrachromosomal telomeric signals are detected in metaphase spreads of all treated MEF lines

• after cre treatment, all mutant MEF lines display multiple chromosome aberrations, including anaphase bridges (16% of cells), chromosomal fusions, breaks, and fragments 35/103 metaphases); in contrast, no anaphase bridges and minimal chromosome aberrations (4/135 metaphases) are observed in control MEFs

• a progressive increase in number of fused chromosomes is seen in all mutant metaphases examined 48-96 hours after cre treatment of MEFs

abnormal cell physiology ( J:112184 )

• cre-treated MEFs display chromosomal instability and form 8-fold more transformed foci compared to control cells

• 4/4 subclones form soft tissue sarcomas following subcutaneous injection into SCID mice

elevated level of mitotic sister chromatid exchange ( J:112184 )

• in cre-treated MEFs, a 4-fold increase in both lagging and leading-strand telomeric-sister chromatid exchange (T-SCE) is observed compared to control virus treated MEFs (Pot1a-sufficient); genomic SCE is not observed above background levels in treated cells

chromosome breakage ( J:112184 )

• chromosome breaks and fragments are found in a significant number of metaphase spreads assayed by telomere PNA-FISH

Genotype
MGI:3715447

cx177

• Allelic Composition: Mdm2^tm1Bay/Mdm2^tm1Mep; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6

hematopoietic system

hematopoietic system phenotype ( J:81065 )

N • thymus is same size as in wild-type mice; thymocytes show wild-type levels of apoptosis and B cells show wild-type levels also

N • number of B220+ B cells in bone marrow is similar to wild-type mice

abnormal bone marrow cell morphology/development ( J:81065 )

• 1.9-fold increase in number of apoptotice B cells relative to wild-type bone marrow

digestive/alimentary system

abnormal small intestine morphology ( J:81065 )

• 17-fold increase in spontaneous apoptosis, occurring mainly in the crypts rather than villi

mortality/aging

decreased mortality induced by ionizing radiation ( J:81065 )

• 100% of animals survive at least 35 days after treatment

homeostasis/metabolism

decreased mortality induced by ionizing radiation ( J:81065 )

• 100% of animals survive at least 35 days after treatment

Genotype
MGI:3763436

cx178

• Allelic Composition: Mdm2^tm1Ypz/Mdm2^tm1Ypz; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6 * FVB/N

mortality/aging

postnatal lethality ( J:126004 )

• no mice are recovered at the time of genotyping

Genotype
MGI:3763437

cx179

• Allelic Composition: Mdm2^tm1Ypz/Mdm2^tm1Ypz; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6 * FVB/N

mortality/aging

mortality/aging ( J:126004 )

N • embryonic lethality observed in Mdm2^tm1Ypz homozygotes is rescued

Genotype
MGI:3712154

cx180

• Allelic Composition: Kat2a^tm1Roth/Kat2a^tm1Roth; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J

mortality/aging

embryonic lethality during organogenesis, incomplete penetrance ( J:121357 )

• double mutants show embryonic lethality similar to Gcnl2-null embryos; numbers of homozygous embryos are normal at E9.5 and 10.5, but reduced relative to expected at E12.5

embryo

embryo phenotype ( J:121357 )

N • embryos have distinct anterior-posterior axis, head folds, and show somite development in contrast to Gcn5l2-null mice; embryos initiate somite and notochord formation, as well as initiation of anterior and midbrain development along the same time frame as in controls

decreased embryonic tissue cell apoptosis ( J:121357 )

• double homozygous embryos show reduced apoptosis relative to Gcn5l2-null single mutants at E8.5-9.0

abnormal embryo turning ( J:121357 )

• double mutants are slow to turn

embryonic growth retardation ( J:121357 )

• embryo development appears delayed at times later than E8.5

decreased embryo size ( J:121357 )

• embryos are smaller than littermates at all time points examined

abnormal somite development ( J:121357 )

• at E8.5, mutant embryos have 1-5 somites compared to littermates which have 7-13 somites

growth/size/body

embryonic growth retardation ( J:121357 )

• embryo development appears delayed at times later than E8.5

decreased embryo size ( J:121357 )

• embryos are smaller than littermates at all time points examined

cellular

decreased embryonic tissue cell apoptosis ( J:121357 )

• double homozygous embryos show reduced apoptosis relative to Gcn5l2-null single mutants at E8.5-9.0

Genotype
MGI:3616344

cx181

• Allelic Composition: Stk11^tm1.1Mlfr/Stk11⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J

mortality/aging

premature death ( J:104347 )

• mice have median age of survival of 4.5 months, similar to Trp53 homozygotes

digestive/alimentary system

colon polyps ( J:104347 )

• 2 of 7 mice have polyps on their lare intestines

neoplasm

increased hamartoma incidence ( J:104347 )

• hamartomatous polyps can be identified at 4.3 months of age, earlier than in double heterozygotes or Stk11 single heterozygotes

Genotype
MGI:3803628

cx182

• Allelic Composition: Mtbp^tm1Glo/Mtbp⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J

mortality/aging

decreased tumor-free survival time ( J:135509 )

• less than 5% of mice live past two years due to cancerous tumors

neoplasm

increased metastatic potential ( J:135509 )

• mice develop significantly more metastatic tumors than Trp53^tm1Tyj heterozygotes (18.2% vs 2.6%)

• metatastic tumors are found in the lung, liver, kidney, and lymph node

• mouse embryonic fibroblasts cells migrate almost as twice as fast as wild-type MEFs through a matrigel membrane

increased tumor incidence ( J:135509 )

• mice develop tumors with age similar to Trp53^tm1Tyj heterozygotes

• over 95% of mice have tumors by 2 years of age

increased leukemia incidence ( J:135509 )

• is observed in 4.5% of mice by 24 months of age

increased lymphoma incidence ( J:135509 )

• is observed in 20.5% of mice by 24 months of age

Genotype
MGI:2183201

cx183

• Allelic Composition: Mdm2^tm1Glo/Mdm2^tm1Glo; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J

normal phenotype

no abnormal phenotype detected ( J:29810 )

Genotype
MGI:3803625

cx184

• Allelic Composition: Mtbp^tm1Glo/Mtbp^tm1Glo; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J

mortality/aging

embryonic lethality between implantation and somite formation, complete penetrance ( J:135509 )

• all embryos die between E3.5 and E7.5

Genotype
MGI:3803626

cx185

• Allelic Composition: Mtbp^tm1Glo/Mtbp^tm1Glo; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J

mortality/aging

embryonic lethality between implantation and somite formation, complete penetrance ( J:135509 )

• all embryos die between E3.5 and E7.5

Genotype
MGI:3616343

cx186

• Allelic Composition: Stk11^tm1.1Mlfr/Stk11⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J

mortality/aging

premature death ( J:104347 )

• Approximately 50% die by 10 months of age, significantly sooner than either single heterozygote

digestive/alimentary system

gastric polyps ( J:104347 )

• time to onset of polyposis is similar to single heterozygotes

• 92% of moribund mice between 7 and 14 months of age have gastrointestinal polyps

• polyps are not found before 5.5 months of age, but at 6.5 months are seen in 60% of mice

growth/size/body

distended abdomen ( J:104347 )

• mice have enlarged abdomens due to presence of polyps in pylorus and duodenum

neoplasm

increased hamartoma incidence ( J:104347 )

• polyps are hamartomas

• tumor-free survival rate is about 11 months compared with 17 months for Trp53 single heterozygotes

• 23 of 38 (61%) of double heterozygotes developed a total of 30 tumors

increased lymphoma incidence ( J:104347 )

• 20% (6 of 30) tumors are lymphomas

increased sarcoma incidence ( J:104347 )

• 10% (3 of 30) of the tumors are sarcomas

increased osteosarcoma incidence ( J:104347 )

• 43% of the tumors (13 of the 30) are osteosarcomas

skeleton

increased osteosarcoma incidence ( J:104347 )

• 43% of the tumors (13 of the 30) are osteosarcomas

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Peutz-Jeghers syndrome		DOID:3852	OMIM:175200	J:104347

Genotype
MGI:2653518

cx187

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Xrcc1^tm1Rpe/Xrcc1^tm1Rpe
• Genetic Background: involves: 129S2/SvPas * 129X1/SvJ

mortality/aging

embryonic lethality, complete penetrance ( J:54226 )

• death by E9.0 to E9.5, 12 to 24 hours after mice homozygous for Xpre1^tm1Rpe alone

embryo

embryonic growth arrest ( J:54226 )

• developmental arrest about 6 h after mice homozygous for Xpre1^tm1Rpe alone

• unlike mice homozygous for Xpre1^tm1Rpe alone, small amounts of mesoderm found

decreased embryo size ( J:54226 )

• but bigger than mice homozygous for Xpre1^tm1Rpe alone

growth/size/body

decreased embryo size ( J:54226 )

• but bigger than mice homozygous for Xpre1^tm1Rpe alone

Genotype
MGI:4360675

cx188

• Allelic Composition: Grid2^Lc-J/Grid2⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129X1/SvJ * BALB/cByJ * C57BL/6

behavior/neurological

ataxia ( J:62117 )

• disruption of Trp53 does not prevent or change the onset of the lurcher ataxia, which is found in the thrid week of life

Genotype
MGI:4888123

cx189

• Allelic Composition: Klf15^tm1Jain/Klf15^tm1Jain; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129X1/SvJ * C57BL/6

cardiovascular system

cardiovascular system phenotype ( J:167880 )

N • responses to angiotensin II infusion are more similar to controls than to the responses in mutant mice wild-type for Trp53

Genotype
MGI:3606184

cx190

• Allelic Composition: Ubr5^tm1Ckww/Ubr5^tm1Ckww; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129X1/SvJ * C57BL/6

mortality/aging

embryonic lethality, complete penetrance ( J:92269 )

• embryos die before E11.5 similar to Edd1 single homozygotes

Genotype
MGI:3694644

cx191

• Allelic Composition: Cdkn2a^tm1Cjs/Cdkn2a^tm1Cjs; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129X1/SvJ * C57BL/6

Persistent hyperplastic primary vitreous (PHPV) in Cdkn2a^tm1Cjs/Cdkn2a^tm1Cjs mice is p53 independent

vision/eye

abnormal eye morphology ( J:75215 )

• exhibit a similar eye phenotype as seen in single Cdkn2a homozygotes that is not altered by the absence of Trp53

abnormal lens capsule morphology ( J:75215 )

• lens capsule destruction to a similar extent as in single Cdkn2a homozygotes

persistent hyperplastic primary vitreous ( J:75215 )

• failure of hyaloid vascular regression similar to that seen in single Cdkn2a homozygotes

Genotype
MGI:4941323

cx192

• Allelic Composition: Rag2^tm2.1Desi/Rag2^tm2.1Desi; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129X1/SvJ * C57BL/6

neoplasm

increased T cell derived lymphoma incidence ( J:168974 )

• in half of mice by 20 weeks, similar to in Trp53^tm1Tyj homozygotes

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:168974 )

• in half of mice by 20 weeks, similar to in Trp53^tm1Tyj homozygotes

Genotype
MGI:4941322

cx193

• Allelic Composition: Rag2^tm1.1Desi/Rag2^tm1.1Desi; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129X1/SvJ * C57BL/6

neoplasm

increased T cell derived lymphoma incidence ( J:168974 )

• unlike in Trp53^tm1Tyj homozygotes, T cell derived lymphomas contain less mature CD4-CD8- and CD4-CD8+ intermediate single positive cells and some lymphomas exhibit chromosomal translocations

increased B cell derived lymphoma incidence ( J:168974 )

• in one fourth of mice

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:168974 )

• unlike in Trp53^tm1Tyj homozygotes, T cell derived lymphomas contain less mature CD4-CD8- and CD4-CD8+ intermediate single positive cells and some lymphomas exhibit chromosomal translocations

Genotype
MGI:3777615

cx194

• Allelic Composition: Dmbt1^tm1Kumc/Dmbt1^tm1Kumc; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * 129X1/SvJ * C57BL/6J

mortality/aging

decreased tumor-free survival time ( J:132597 )

• majority of mice (86%) die early (before 9 months of age), or are euthanized due to occurrence of obvious tumor mass

neoplasm

neoplasm ( J:132597 )

N • mice do not develop tumors in pancreas or gastrointestinal tract regardless of Trp53 status

Genotype
MGI:3777616

cx195

• Allelic Composition: Dmbt1^tm1Kumc/Dmbt1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * 129X1/SvJ * C57BL/6J

mortality/aging

decreased tumor-free survival time ( J:132597 )

• some mice die before 9 month experimental end-point of 9 months due to development of obvious tumor mass

Genotype
MGI:3663690

cx196

• Allelic Composition: Nf1^tm1Tyj/?; Nstr1^A/J/?; Trp53^tm1Tyj/?
• Genetic Background: involves: 129S2/SvPas * A/J * C57BL/6J

neoplasm

decreased tumor incidence ( J:105038 )

• resistance to peripheral nerve sheath tumors

Genotype
MGI:3663691

cx197

• Allelic Composition: Nf1^tm1Tyj/?; Nstr1^C57BL/6J/Nstr1^C57BL/6J; Trp53^tm1Tyj/?
• Genetic Background: involves: 129S2/SvPas * A/J * C57BL/6J

neoplasm

increased neurofibrosarcoma incidence ( J:105038 )

• susceptibility to developing peripheral nerve sheath tumors

nervous system

increased neurofibrosarcoma incidence ( J:105038 )

• susceptibility to developing peripheral nerve sheath tumors

Genotype
MGI:3663692

cx198

• Allelic Composition: Nf1^tm1Tyj/?; Nstr2^A/J/?; Trp53^tm1Tyj/?
• Genetic Background: involves: 129S2/SvPas * A/J * C57BL/6J

neoplasm

decreased tumor incidence ( J:105038 )

• resistance to peripheral nerve sheath tumors

Genotype
MGI:3700821

cx199

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Wrn^tm1Lgu/Wrn^tm1Lgu
• Genetic Background: involves: 129S2/SvPas * BALB/c

mortality/aging

premature death ( J:61567 )

• double mutants exhibit increased mortality rate (life span of 122 days) relative to mice homozygous for Trp53^tm1Tyj and heterozygous for Wrn^tm1Lgu (life span of 149 days)

Genotype
MGI:5500165

cx200

• Allelic Composition: Rps7^Zma/Rps7⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * BALB/c * C3H/HeH * C57BL/6J

Increased apoptosis in the developing central nervous system of Rps7^Zma/Rps7⁺ embryos which is reduced in Rps7^Zma/Rps7⁺ Trp53^tm1Tyj/Trp53⁺ embryos

mortality/aging

mortality/aging ( J:195156 )

N • viability is restored compared to in Rps7^Zma heterozygotes

pigmentation

belly spot ( J:195156 )

• small belly spot in some mice

embryo

embryo phenotype ( J:195156 )

N • embryonic developmental delay observed in Rps7^Zma heterozygotes is suppressed

hematopoietic system

hematopoietic system phenotype ( J:195156 )

N • erythroid maturation defects observed in Rps7^Zma heterozygotes are suppressed

integument

belly spot ( J:195156 )

• small belly spot in some mice

limbs/digits/tail

limbs/digits/tail phenotype ( J:195156 )

N • tail kinks observed in Rps7^Zma heterozygotes are suppressed

nervous system

nervous system phenotype ( J:195156 )

N • neuron apoptosis observed in Rps7^Zma heterozygotes is suppressed

skeleton

skeleton phenotype ( J:195156 )

N • vertebral fusions observed in Rps7^Zma heterozygotes are suppressed

Genotype
MGI:6192108

cx201

• Allelic Composition: Tg(Ela1-Tgfa)150Bri/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * BALB/c * C57BL/6 * SJL

endocrine/exocrine glands

increased pancreas tumor incidence ( J:67389 )

• 100% of mice develop pancreatic tumors within 120 days after birth

increased pancreatic ductal adenocarcinoma incidence ( J:67389 )

• pancreatic carcinomas display a ductal phenotype, grow invasively into surrounding tissue, and metastasize

neoplasm

increased pancreas tumor incidence ( J:67389 )

• 100% of mice develop pancreatic tumors within 120 days after birth

increased pancreatic ductal adenocarcinoma incidence ( J:67389 )

• pancreatic carcinomas display a ductal phenotype, grow invasively into surrounding tissue, and metastasize

increased malignant tumor incidence ( J:67389 )

• pancreatic carcinomas metastasize to liver and lung

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
pancreatic carcinoma		DOID:4905	OMIM:260350	J:67389

Genotype
MGI:6192107

cx202

• Allelic Composition: Tg(Ela1-Tgfa)150Bri/0; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * BALB/c * C57BL/6 * SJL

endocrine/exocrine glands

increased pancreas tumor incidence ( J:67389 )

• 77.3% of mice develop pancreatic tumors with a mean tumor-free survival of 220 days

• tumors sometimes show loss of heterozygosity for Trp53, Inkra/Arf, and/or Smad4

neoplasm

increased pancreas tumor incidence ( J:67389 )

• 77.3% of mice develop pancreatic tumors with a mean tumor-free survival of 220 days

• tumors sometimes show loss of heterozygosity for Trp53, Inkra/Arf, and/or Smad4

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
pancreatic carcinoma		DOID:4905	OMIM:260350	J:67389

Genotype
MGI:5463922

cx203

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Uimc1^tm1.2Amj/Uimc1^tm1.2Amj
• Genetic Background: involves: 129S2/SvPas * BALB/cJ * C57BL/6

mortality/aging

decreased tumor-free survival time ( J:191827 )

• significant decrease in tumor free survival

Genotype
MGI:5463923

cx204

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺; Uimc1^tm1.2Amj/Uimc1^tm1.2Amj
• Genetic Background: involves: 129S2/SvPas * BALB/cJ * C57BL/6

neoplasm

increased tumor growth/size ( J:191827 )

• weight of ionizing radiation induced thymic lymphomas is increased compared to mutant mice wild-type for Uimc1

increased lymphoma incidence ( J:191827 )

• 78.5% of mice (11 of 14) develop thymic lymphomas after exposure to ionizing radiation

increased incidence of tumors by ionizing radiation induction ( J:191827 )

• 78.5% of mice (11 of 14) develop thymic lymphomas after exposure to ionizing radiation

Genotype
MGI:3715519

cx205

• Allelic Composition: Suprmam1^BALB/cMed/Suprmam1^BALB/cMed; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * BALB/cMed * C57BL/6 * C57BL/6J

neoplasm

increased mammary gland tumor incidence ( J:122161 )

• decreased tumor latency by 10 weeks

• 2-fold increased mammary tumor risk

• increased mammary tumor incidence

• decreased mammary tumor-free survival

integument

increased mammary gland tumor incidence ( J:122161 )

• decreased tumor latency by 10 weeks

• 2-fold increased mammary tumor risk

• increased mammary tumor incidence

• decreased mammary tumor-free survival

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:122161 )

• decreased tumor latency by 10 weeks

• 2-fold increased mammary tumor risk

• increased mammary tumor incidence

• decreased mammary tumor-free survival

Genotype
MGI:3799500

cx206

• Allelic Composition: Tg(K6ODCtr)55Tgo/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C3H * C57BL/6

cellular

cellular phenotype ( J:133302 )

N • in culture, primary keratinocytes exhibit normal life span

Genotype
MGI:6260021

cx207

• Allelic Composition: Rps20^Mhdadsk4/Rps20⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C3HeB/FeJ

pigmentation

pigmentation phenotype ( J:139244 )

N • adult mice exhibit reversal of the hyperpigmentation phenotype seen in the footpad and tail skin of single Rps20^Mhdadsk4 heterozygotes

Genotype
MGI:6260014

cx208

• Allelic Composition: Rps19^Mhdadsk3/Rps19⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C3HeB/FeJ

pigmentation

pigmentation phenotype ( J:139244 )

N • adult mice exhibit reversal of the hyperpigmentation phenotype seen in the footpad and tail skin of single Rps19^Mhdadsk3 heterozygotes

growth/size/body

growth/size/body region phenotype ( J:139244 )

N • adult mice exhibit reversal of the body weight phenotypes seen in single Rps19^Mhdadsk3 heterozygotes

hematopoietic system

abnormal hematopoietic system morphology/development ( J:139244 )

• adult mice exhibit reversal of the erythrocyte phenotype seen in single Rps19^Mhdadsk3 heterozygotes

Genotype
MGI:5302543

cx209

• Allelic Composition: Pclaf^tm1.1Lkd/Pclaf^tm1.1Lkd; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6

hematopoietic system

increased hematopoietic stem cell number ( J:177782 )

• lymphoid-primed multipotent progenitors are increased compared to in 2810417H13Rik^tm1.1Lkd homozygotes

Genotype
MGI:4839564

cx210

• Allelic Composition: Pknox1^tm1Fbla/Pknox1^tm1Fbla; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

embryonic lethality, complete penetrance ( J:165811 )

• mice are almost reabsorbed between E9.5 and E10.5

embryo

abnormal embryo development ( J:165811 )

• anterior visceral endoderm and primitive streak formation are partially rescued compared to in Pknox1^tm1Fbla homozygotes

embryonic growth retardation ( J:165811 )

• at E8.5

abnormal embryonic epiblast morphology ( J:165811 )

abnormal pluripotent precursor cell morphology ( J:165811 )

• the Oct4 expression domain is expanded with a decrease in apoptosis compared to in Pknox1^tm1Fbla homozygotes

abnormal extraembryonic endoderm formation ( J:165811 )

• the extra-embryonic ectoderm is better organized than in Pknox1^tm1Fbla homozygotes

growth/size/body

embryonic growth retardation ( J:165811 )

• at E8.5

Genotype
MGI:3032768

cx211

• Allelic Composition: Thbs1^tm1Hyn/Thbs1^tm1Hyn; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:72391 )

• average life span of 426 days

neoplasm

increased pancreas tumor incidence ( J:72391 )

• 1.6% incidence of pancreatic adenocarcinomas

• 1.6% incidence of islet cell adenocarcinomas

abnormal tumor morphology ( J:72391 )

• 58% of 19 tumors exhibit loss of heterozygosity for Trp53

increased adenoma incidence ( J:72391 )

• 4.7% incidence

increased lymphoma incidence ( J:72391 )

• 44% incidence

increased histiocytic sarcoma incidence ( J:72391 )

• 17% incidence

increased carcinoma incidence ( J:72391 )

• 33% incidence

increased adenocarcinoma incidence ( J:72391 )

• 19% incidence of adenocarcinomas

• 1.6% incidence of pancreatic adenocarcinomas

• 1.6% incidence of islet cell adenocarcinomas

increased mammary adenocarcinoma incidence ( J:72391 )

• 4.7% incidence

increased liver adenocarcinoma incidence ( J:72391 )

• 1.6% incidence of hepatocarcinoma

increased lung adenocarcinoma incidence ( J:72391 )

• 9.4% incidence

increased squamous cell carcinoma incidence ( J:72391 )

• 14% incidence of ear squamous cell carcinoma

increased sarcoma incidence ( J:72391 )

• 44% incidence of sarcomas

• 1.6% incidence of undifferentiated sarcomas

increased fibrosarcoma incidence ( J:72391 )

• 13% incidence

increased osteosarcoma incidence ( J:72391 )

• 13% incidence

increased papilloma incidence ( J:72391 )

• 1.6% incidence of stomach papilloma

digestive/alimentary system

gastric polyps ( J:72391 )

• 13% incidence of stomach polyps

respiratory system

increased lung adenocarcinoma incidence ( J:72391 )

• 9.4% incidence

integument

increased mammary adenocarcinoma incidence ( J:72391 )

• 4.7% incidence

liver/biliary system

increased liver adenocarcinoma incidence ( J:72391 )

• 1.6% incidence of hepatocarcinoma

skeleton

increased osteosarcoma incidence ( J:72391 )

• 13% incidence

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:72391 )

• 4.7% incidence

increased pancreas tumor incidence ( J:72391 )

• 1.6% incidence of pancreatic adenocarcinomas

• 1.6% incidence of islet cell adenocarcinomas

Genotype
MGI:6715104

cx212

• Allelic Composition: Fdxr^tm1Xch/Fdxr⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6

homeostasis/metabolism

abnormal iron level ( J:244082 )

• mild iron overload in E8.0 embryos

Genotype
MGI:3770520

cx213

• Allelic Composition: Kras^tm2Tyj/Kras⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:68981 )

neoplasm

increased tumor incidence ( J:68981 )

• double mutants display more malignant features than Kras heterozygous tumors, with marked cellular pleomorphism and anaplastic changes with giant cell formation

• mice have broader tumor spectrum compared to Kras or Trp53 heterozygotes, including histocytic sarcoma, medulloblastoma, osteosarcoma, and teratoma

increased T cell derived lymphoma incidence ( J:68981 )

increased skin papilloma incidence ( J:68981 )

increased fibrosarcoma incidence ( J:68981 )

increased hemangiosarcoma incidence ( J:68981 )

integument

increased skin papilloma incidence ( J:68981 )

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:68981 )

Genotype
MGI:6715105

cx214

• Allelic Composition: Fdxr^tm1Xch/Fdxr⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

homeostasis/metabolism

abnormal iron level ( J:244082 )

• mild iron overload in E8.0 embryos

Genotype
MGI:5475167

cx215

• Allelic Composition: Nhej1^tm1.1Ics/Nhej1^tm1.1Ics; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

immune system

decreased thymocyte apoptosis ( J:194422 )

• compared with cells from Nhej1^tm1.1Ics homozygotes and heterozygotes

abnormal T cell receptor V(D)J recombination ( J:194422 )

• Jalpha and Valpha usage are partially normalized

decreased NK T cell number ( J:194422 )

• partially recovery of invariant NK T cell numbers compared to in Nhej1^tm1.1Ics homozygotes

cellular

decreased thymocyte apoptosis ( J:194422 )

• compared with cells from Nhej1^tm1.1Ics homozygotes and heterozygotes

hematopoietic system

decreased thymocyte apoptosis ( J:194422 )

• compared with cells from Nhej1^tm1.1Ics homozygotes and heterozygotes

abnormal T cell receptor V(D)J recombination ( J:194422 )

• Jalpha and Valpha usage are partially normalized

decreased NK T cell number ( J:194422 )

• partially recovery of invariant NK T cell numbers compared to in Nhej1^tm1.1Ics homozygotes

endocrine/exocrine glands

decreased thymocyte apoptosis ( J:194422 )

• compared with cells from Nhej1^tm1.1Ics homozygotes and heterozygotes

Genotype
MGI:3770519

cx216

• Allelic Composition: Kras^tm2Tyj/Kras⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:68981 )

• mice have reduced life spans compared to Kras or Trp53 heterozygous mice, or Trp53 homozygotes

neoplasm

increased tumor incidence ( J:68981 )

• double mutants display more malignant features than Kras heterozygous tumors, with marked cellular pleomorphism and anaplastic changes with giant cell formation

• mice have broader tumor spectrum compared to Kras or Trp53 heterozygotes, including histocytic sarcoma, medulloblastoma, osteosarcoma, and teratoma

increased T cell derived lymphoma incidence ( J:68981 )

• Background Sensitivity: about 40% of animals develop thymic lymphoma; incidence is higher than on pure 129/Sv background

increased skin papilloma incidence ( J:68981 )

• about 40% of mice develop skin papillomas, with slightly higher incidence than on mixed 129 and C57BL/6 background

increased fibrosarcoma incidence ( J:68981 )

• about 30% of double mutants develop fibrosarcoma

increased hemangiosarcoma incidence ( J:68981 )

• about 30% of double mutants develop hemangiosarcoma

integument

increased skin papilloma incidence ( J:68981 )

• about 40% of mice develop skin papillomas, with slightly higher incidence than on mixed 129 and C57BL/6 background

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:68981 )

• Background Sensitivity: about 40% of animals develop thymic lymphoma; incidence is higher than on pure 129/Sv background

Genotype
MGI:3700989

cx217

• Allelic Composition: Fos^tm1Wag/Fos^tm1Wag; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

skeleton

osteopetrosis ( J:89283 )

• double mutants display similar osteopetrotic phenotype to Fos^tm1Wag mice

neoplasm

increased rhabdomyosarcoma incidence ( J:89283 )

• at 10 weeks of age, double mutants develop facial and orbital tumors with penetrance of 93% at 25 weeks of age

• tumors are polygonal or elongated with pleomorphic nuclei and eosinophilic cytoplasm with cross-striations

• tumors display invasive growth into facial and external orbital muscles

muscle

increased rhabdomyosarcoma incidence ( J:89283 )

• at 10 weeks of age, double mutants develop facial and orbital tumors with penetrance of 93% at 25 weeks of age

• tumors are polygonal or elongated with pleomorphic nuclei and eosinophilic cytoplasm with cross-striations

• tumors display invasive growth into facial and external orbital muscles

Genotype
MGI:5523485

cx218

• Allelic Composition: Exo1^tm2Wed/Exo1^tm2Wed; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:198719 )

• compared with Trp53^tm1Tyj homozygotes

neoplasm

increased tumor incidence ( J:198719 )

• tumor spectrum is the same as in Trp53^tm1Tyj homozygotes

cellular

chromosomal instability ( J:198719 )

• less segmental chromosomal instability than in Trp53^tm1Tyj homozygotes

Genotype
MGI:5523487

cx219

• Allelic Composition: Exo1^tm3.1Wed/Exo1^tm3.1Wed; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:198719 )

• survival is similar to in Trp53^tm1Tyj homozygotes

neoplasm

increased lymphoma incidence ( J:198719 )

• but less than in Trp53^tm1Tyj homozygotes

increased sarcoma incidence ( J:198719 )

• compared with Trp53^tm1Tyj homozygotes

cellular

abnormal chromosome stability ( J:198719 )

• mice exhibit the same amount of segmental chromosomal instability as in Trp53^tm1Tyj homozygotes

Genotype
MGI:3700990

cx220

• Allelic Composition: Fos^tm1Wag/Fos^tm1Wag; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6

neoplasm

increased rhabdomyosarcoma incidence ( J:89283 )

• double mutants develop facial and orbital tumors with lower penetrance than in double homozygous mice

muscle

increased rhabdomyosarcoma incidence ( J:89283 )

• double mutants develop facial and orbital tumors with lower penetrance than in double homozygous mice

Genotype
MGI:3032769

cx221

• Allelic Composition: Thbs1^tm1Hyn/Thbs1^tm1Hyn; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:72391 )

• average life span of 149 days

neoplasm

increased pancreas tumor incidence ( J:72391 )

• 2.8% incidence of pancreas adenocarcinoma

increased lymphoma incidence ( J:72391 )

• 53% incidence

increased histiocytic sarcoma incidence ( J:72391 )

• 5.6% incidence

increased carcinoma incidence ( J:72391 )

• 8.3% incidence

increased adenocarcinoma incidence ( J:72391 )

• 5.6% incidence of adenocarcinoma

• 2.8% incidence of pancreas adenocarcinoma

increased small intestine adenocarcinoma incidence ( J:72391 )

• 2.8% incidence

increased sarcoma incidence ( J:72391 )

• 39% incidence of sarcomas, however no osteosarcomas are seen as in single Trp53 mutants

• 5.6% incidence of undifferentiated sarcoma

increased fibrosarcoma incidence ( J:72391 )

• 8.3% incidence

increased hemangiosarcoma incidence ( J:72391 )

• 17% incidence

digestive/alimentary system

increased small intestine adenocarcinoma incidence ( J:72391 )

• 2.8% incidence

endocrine/exocrine glands

increased pancreas tumor incidence ( J:72391 )

• 2.8% incidence of pancreas adenocarcinoma

Genotype
MGI:2653312

cx222

• Allelic Composition: Tfdp1^tm1Lili/Tfdp1⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

prenatal lethality, incomplete penetrance ( J:81580 )

• incomplete penetrance, ~50% survive to adulthood

nervous system

exencephaly ( J:81580 )

• observed at E13.5, and incompletely penetrant

Genotype
MGI:5699872

cx223

• Allelic Composition: Nf1^tm1Tyj/Nf1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:217077 , J:228258 )

• most mice die by 250 days (J:217077)

• median survival time is 5-15 months (J:228258)

immune system

spleen hyperplasia ( J:228258 )

• 41.2% of mice exhibit splenic hyperplasia

neoplasm

increased metastatic potential ( J:228258 )

• metastases are seen in 29.4% of mice with sarcomas

increased tumor incidence ( J:217077 )

increased lymphoma incidence ( J:217077 , J:228258 )

• 3% of mice develop lymphomas (J:217077)

• mice develop lymphomas around 3-6 months of age (J:228258)

increased histiocytic sarcoma incidence ( J:217077 )

• 10% of mice develop histiocytic sarcomas

increased neuroblastoma incidence ( J:217077 )

• 8% of mice develop neuroblastoma

increased sarcoma incidence ( J:228258 )

• 59.5% of mice develop soft tissue sarcomas of the limbs and abdomen around 3-6 months of age

increased neurofibrosarcoma incidence ( J:217077 )

• 67% of mice develop malignant peripheral nerve sheath tumors

• tumors develop on average at 150 days of age

increased glioma incidence ( J:217077 )

• 15% of mice develop high-grade glioma

• gliomas develop at approximately 200 days of age

nervous system

increased neuroblastoma incidence ( J:217077 )

• 8% of mice develop neuroblastoma

increased neurofibrosarcoma incidence ( J:217077 )

• 67% of mice develop malignant peripheral nerve sheath tumors

• tumors develop on average at 150 days of age

increased glioma incidence ( J:217077 )

• 15% of mice develop high-grade glioma

• gliomas develop at approximately 200 days of age

hematopoietic system

spleen hyperplasia ( J:228258 )

• 41.2% of mice exhibit splenic hyperplasia

growth/size/body

spleen hyperplasia ( J:228258 )

• 41.2% of mice exhibit splenic hyperplasia

Genotype
MGI:2653311

cx224

• Allelic Composition: Tfdp1^tm1Lili/Tfdp1^tm1Lili; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

prenatal lethality, complete penetrance ( J:81580 )

Genotype
MGI:3041266

cx225

• Allelic Composition: Prdm2^tm1Shg/Prdm2^tm1Shg; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:71406 )

• mean age of survival was 415 days vs. mice heterozygous for Trp53^tm1Tyj alone or homozygous Prdm2^tm1Shg alone, which survived to ~550 days

neoplasm

increased tumor incidence ( J:71406 )

• of types similar to those found in mice homozygous for Prdm2^tm1Shg alone

Genotype
MGI:6358197

cx226

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺; Utp25^em1Glo/Utp25^em1Glo
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

embryonic lethality between implantation and somite formation, complete penetrance ( J:272648 )

• no embryos found at ages E7.5, E9.5, E17.5 and no mice at age P21

• empty decidua found at ages E7.5 and E9.5

Genotype
MGI:6358195

cx227

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Utp25^em1Glo/Utp25^em1Glo
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

embryonic lethality between implantation and somite formation, complete penetrance ( J:272648 )

• no embryos found at ages E7.5, E9.5, E17.5 and no mice at age P21

• empty decidua found at ages E7.5 and E9.5

Genotype
MGI:3582787

cx228

• Allelic Composition: Rb1^tm1Tyj/Rb1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:19542 )

• the mean age of survival of double heterozygotes is slightly reduced relative to mice heterozygous for Rb1^tm1Tyj alone (9 months vs 11 months)

neoplasm

abnormal tumor morphology ( J:19542 )

• in nearly all double heterozygotes with pituitary and thyroid tumors, the wild-type allele of Rb1 is lost whereas the wild-type allele of Trp53 is retained

increased tumor incidence ( J:19542 )

• one of 7 individual double heterozygotes analyzed displayed a single pinealoblastoma (not detected in single heterozygotes); the wild-type alleles of both Rb1 and Trp53 were lost in this pineal tumor

increased pancreatic islet cell carcinoma incidence ( J:19542 )

• 14% of a total of 14 individual double heterozygotes analyzed displayed islet cell carcinomas (not detected in single heterozygotes)

• notably, the wild-type alleles of both Rb1 and Trp53 were lost in tumors of the islet cells of the pancreas

increased pituitary melanotroph tumor incidence ( J:19542 )

• each of 67 double heterozygotes analyzed developed pituitary tumors of the intermediate lobe

increased thyroid tumor incidence ( J:19542 )

• ~75% of double heterozygous mice develop medullary thyroid tumors

increased sarcoma incidence ( J:19542 )

• 6% of a total of 67 individual double heterozygotes analyzed displayed anaplastic sarcomas

• such tumors were shown to be more aggressive and arise at an earlier age than those occurring in single Trp53^tm1Tyj heterozygotes

• notably, the wild-type alleles of both Rb1 and Trp53 were lost in these anaplastic sarcomas

increased leiomyosarcoma incidence ( J:19542 )

• one of 7 individual double heterozygotes analyzed displayed a leiomyosarcoma

respiratory system

bronchial epithelial hyperplasia ( J:19542 )

• 8% of a total of 12 individual double heterozygotes analyzed displayed bronchial hyperplasia

muscle

increased leiomyosarcoma incidence ( J:19542 )

• one of 7 individual double heterozygotes analyzed displayed a leiomyosarcoma

endocrine/exocrine glands

increased pancreatic islet cell carcinoma incidence ( J:19542 )

• 14% of a total of 14 individual double heterozygotes analyzed displayed islet cell carcinomas (not detected in single heterozygotes)

• notably, the wild-type alleles of both Rb1 and Trp53 were lost in tumors of the islet cells of the pancreas

increased pituitary melanotroph tumor incidence ( J:19542 )

• each of 67 double heterozygotes analyzed developed pituitary tumors of the intermediate lobe

increased thyroid tumor incidence ( J:19542 )

• ~75% of double heterozygous mice develop medullary thyroid tumors

nervous system

increased pituitary melanotroph tumor incidence ( J:19542 )

• each of 67 double heterozygotes analyzed developed pituitary tumors of the intermediate lobe

Genotype
MGI:5141752

cx229

• Allelic Composition: Mdm4^tm1Zmy/Mdm4^tm1Zmy; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

normal phenotype

no abnormal phenotype detected ( J:174359 )

• phenotypes are almost identical to control littermates

Genotype
MGI:5319199

cx230

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(CAG-EGFP/Map1lc3b)53Nmz/0
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * C57BL/6NCrj

cardiovascular system

abnormal heart morphology ( J:183674 )

• following permanent coronary artery ligation, mice exhibit decreased apoptotic myocyte death and improved cardiac remodeling (smaller fibrotic lesions, decreased cardiac hyperplasia, improved left ventricle size and contractility and decreased accumulation of damaged mitochondria) compared with wild-type mice

increased cardiac muscle contractility ( J:183674 )

• following myocardial infarction

decreased cardiomyocyte apoptosis ( J:183674 )

• following myocardial infarction

abnormal response to cardiac infarction ( J:183674 )

• following permanent coronary artery ligation, mice exhibit decreased apoptotic myocyte death and improved cardiac remodeling (smaller fibrotic lesions, decreased cardiac hyperplasia, improved left ventricle size and contractility and decreased accumulation of damaged mitochondria) compared with wild-type mice

• following myocardial infarction, cardiac muscles exhibit increased autophagy, levels of reactive oxygen species production mitophagy and decreased mitochondria DNA damage compared to in wild-type mice

cellular

decreased cardiomyocyte apoptosis ( J:183674 )

• following myocardial infarction

abnormal mitochondrial chromosome morphology ( J:183674 )

• following myocardial infarction, cardiac muscles exhibit decreased mitochondria DNA damage compared to in wild-type mice

• however, treatment with chloroquine elevates mitochondria DNA damage to wild-type levels

abnormal autophagy ( J:183674 )

• following myocardial infarction, autophagy in cardiac muscles is increased compared to in wild-type mice

abnormal mitochondrial physiology ( J:183674 )

• following myocardial infarction, cardiac muscles exhibit increased mitophagy compared to in wild-type mice

• however, treatment with chloroquine elevates mitochondrial to wild-type levels

oxidative stress ( J:183674 )

• following myocardial infarction, cardiac muscles exhibit increased levels of reactive oxygen species production compared to in wild-type mice

homeostasis/metabolism

abnormal response to cardiac infarction ( J:183674 )

• following permanent coronary artery ligation, mice exhibit decreased apoptotic myocyte death and improved cardiac remodeling (smaller fibrotic lesions, decreased cardiac hyperplasia, improved left ventricle size and contractility and decreased accumulation of damaged mitochondria) compared with wild-type mice

• following myocardial infarction, cardiac muscles exhibit increased autophagy, levels of reactive oxygen species production mitophagy and decreased mitochondria DNA damage compared to in wild-type mice

abnormal autophagy ( J:183674 )

• following myocardial infarction, autophagy in cardiac muscles is increased compared to in wild-type mice

muscle

increased cardiac muscle contractility ( J:183674 )

• following myocardial infarction

decreased cardiomyocyte apoptosis ( J:183674 )

• following myocardial infarction

Genotype
MGI:5609812

cx231

• Allelic Composition: Cenpj^{tm1d(EUCOMM)Wtsi}/Cenpj^{tm1d(EUCOMM)Wtsi}; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * C57BL/6N * FVB/NJ
• Cell Lines: EPD0028_7_G05

embryo

embryo phenotype ( J:208632 )

N • survive until at least E9.5 and complete embryonic turning

abnormal dorsal-ventral axis patterning ( J:208632 )

• absence of ventral neural cell types that depend on high or intermediated SHH signaling levels and expansion of markers that are normally repressed by SHH into the ventral neural tube

abnormal neural tube morphology ( J:208632 )

• absence of ventral neural cell types that depend on high or intermediated SHH signaling levels and expansion of markers that are normally repressed by SHH into the ventral neural tube

abnormal embryonic neuroepithelium morphology ( J:208632 )

• lack centrioles at E8.5 even in mitotic cells in metaphase conformation

nervous system

abnormal neural tube morphology ( J:208632 )

• absence of ventral neural cell types that depend on high or intermediated SHH signaling levels and expansion of markers that are normally repressed by SHH into the ventral neural tube

abnormal embryonic neuroepithelium morphology ( J:208632 )

• lack centrioles at E8.5 even in mitotic cells in metaphase conformation

cellular

abnormal centrosome morphology ( J:208632 )

• disrupted organization of the centrosome in MEFs

abnormal mitosis ( J:208632 )

• disrupted organization of the centrosome in MEFs

• astral microtubules are present but decreased in number in MEFs

• no signs of increased aneuploidy are detected

abnormal apoptosis ( J:208632 )

• number of apoptotic cells is reduced compared to mice homozygous for Cenpj^{tm1b(EUCOMM)Wtsi} alone

Genotype
MGI:5432018

cx232

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(Ly6e-MALT1)#Isg/0
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * CBA

Tg(Ly6e-MALT1)#Isg/0 Trp53^tm1Tyj/Trp53^tm1Tyj mice develop activated B-cell diffuse large-cell lymphoma

mortality/aging

premature death ( J:185590 )

• die earlier than transgenic mice wild-type for Trp53

neoplasm

increased B cell derived lymphoma incidence ( J:185590 )

• develop aggressive lymphomas characterized by a diffuse infiltrate of large B-lymphocytes with nuclei with dispersed chromatin, deeply basophilic cytoplasm and multiple mitotic figures

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
diffuse large B-cell lymphoma		DOID:0050745		J:185590

Genotype
MGI:5430234

cx233

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Tg(Prrx1-FUS/DDIT3)1Mete/0
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * CBA

neoplasm

increased sarcoma incidence ( J:184491 )

• predominantly in the appendicular skeleton

increased liposarcoma incidence ( J:184491 )

• mice develop myxoid round cell liposarcoma

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
myxoid liposarcoma		DOID:5363	OMIM:613488	J:184491

Genotype
MGI:5751688

cx234

• Allelic Composition: Tg(Trp53)1Srn/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * CBA

cellular

decreased thymocyte apoptosis ( J:80311 )

• radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53^tm1Tyj mice, but is decreased as compared to wild-type, and is similar to heterozygous Trp53^tm1Tyj mice

endocrine/exocrine glands

decreased thymocyte apoptosis ( J:80311 )

• radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53^tm1Tyj mice, but is decreased as compared to wild-type, and is similar to heterozygous Trp53^tm1Tyj mice

hematopoietic system

decreased thymocyte apoptosis ( J:80311 )

• radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53^tm1Tyj mice, but is decreased as compared to wild-type, and is similar to heterozygous Trp53^tm1Tyj mice

immune system

decreased thymocyte apoptosis ( J:80311 )

• radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53^tm1Tyj mice, but is decreased as compared to wild-type, and is similar to heterozygous Trp53^tm1Tyj mice

mortality/aging

premature death ( J:80311 )

• average lifespan is 9.5 months

• mice live longer than homozygous Trp53^tm1Tyj mice (4.5 months)

• but, not as long as heterozygous Trp53^tm1Tyj mice (14 months)

Genotype
MGI:4836242

cx235

• Allelic Composition: Tg(Pbsn-TAg)15Tvd/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * DBA/2

endocrine/exocrine glands

abnormal prostate gland epithelium morphology ( J:103408 )

♂ • proliferation and apoptosis in the prostate remains similar to single transgenic Tg(Pbsn-TAg)15Tvd mice

reproductive system

abnormal prostate gland epithelium morphology ( J:103408 )

♂ • proliferation and apoptosis in the prostate remains similar to single transgenic Tg(Pbsn-TAg)15Tvd mice

Genotype
MGI:3698864

cx236

• Allelic Composition: Suds3^tm1.1Rdp/Suds3⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB

neoplasm

decreased tumor incidence ( J:117829 )

• mice show a suppression of the cancer phenotype compared to Sds-haploinsufficinet, Trp53-null mice

Genotype
MGI:3698865

cx237

• Allelic Composition: Sin3a^tm1.1Rdp/Sin3a⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB

neoplasm

neoplasm ( J:117829 )

N • mice show identical tumor incidence, tumor multiplicity, and tumor spectrum to mice with a Sin3a-sufficient, Trp53-null background

Genotype
MGI:3698863

cx238

• Allelic Composition: Suds3^tm1.1Rdp/Suds3⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB

cellular

aneuploidy ( J:117829 )

• tumor cells in primary cultures are typically aneuploid with chromosome counts of 30 to >100; tumors from controls are usually euploid

• tumor metaphases posess multi-radial chromosomes and sometimes more than 3 chromosomes are associated through their centromeric regions

neoplasm

increased tumor incidence ( J:117829 )

• compared to Suds3-sufficient Trp53-null mice, mice show increased tumor multiplicity per mouse (2.45 vs 1.2 macroscopic tumors)

decreased tumor latency ( J:117829 )

• compared to Suds3-sufficient Trp53-null mice, mice show accelerated tumor onset (latency of 12.3 vs 13.9 weeks)

Genotype
MGI:5316383

cx239

• Allelic Composition: Pum1^tm1.2Hfl/Pum1^tm1.2Hfl; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB

reproductive system

reproductive system phenotype ( J:182280 )

N • testis hypotrophy and male germ cell apoptosis are rescued

small seminiferous tubules ( J:182280 )

♂ • not as much as in Pum1^tm1.2Hfl homozygotes

endocrine/exocrine glands

small seminiferous tubules ( J:182280 )

♂ • not as much as in Pum1^tm1.2Hfl homozygotes

Genotype
MGI:5688514

cx240

• Allelic Composition: Rbm38^tm1.1Xch/Rbm38^tm1.1Xch; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB/N

mortality/aging

decreased mortality induced by ionizing radiation ( J:216929 )

• median survival following exposure to 8 gray of whole body gamma-irradiation is 34 days similar to mutant mice wild-type for Rbm38

premature death ( J:216929 )

• longest lifespan is 29 weeks, median survival is 19 weeks

neoplasm

abnormal tumor susceptibility ( J:216929 )

• tumor spectrum is significantly different from mutant mice wild-type for Rbm38

• mice do not develop hibernoma or hemangioma

increased lymphoma incidence ( J:216929 )

• compared to mutant mice wild-type for Rbm38 (94.1% vs 60.6%)

decreased tumor incidence ( J:216929 )

• tumor burden is markedly reduced compared to mutant mice wild-type for Rbm38 with no mice developing more than 1 primary tumor

decreased sarcoma incidence ( J:216929 )

• compared to mutant mice wild-type for Rbm38 (5.8% vs 30.3%)

decreased tumor latency ( J:216929 )

• tumor onset is 15 weeks compared to 18 weeks in mutant mice wild-type for Rbm38

homeostasis/metabolism

decreased mortality induced by ionizing radiation ( J:216929 )

• median survival following exposure to 8 gray of whole body gamma-irradiation is 34 days similar to mutant mice wild-type for Rbm38

Genotype
MGI:5688515

cx241

• Allelic Composition: Rbm38^tm1.1Xch/Rbm38^tm1.1Xch; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB/N

mortality/aging

premature death ( J:216929 )

• median survival is 70 weeks, slightly but not statistically significantly longer than in mutant mice wild-type for Rbm38

neoplasm

abnormal tumor susceptibility ( J:216929 )

• tumor spectrum is slightly different from mutant mice wild-type for Rbm38

decreased tumor incidence ( J:216929 )

• 9 of 21 mice do not succumb to tumors compared to 1 of 24 mutant mice wild-type for Rbm38

hematopoietic system

abnormal spleen B cell follicle morphology ( J:216929 )

• splenic follicular hyperplasia in tumor free mice

liver/biliary system

hepatic steatosis ( J:216929 )

• in tumor free mice

immune system

abnormal spleen B cell follicle morphology ( J:216929 )

• splenic follicular hyperplasia in tumor free mice

Genotype
MGI:6152435

cx242

• Allelic Composition: Rbm24^tm1.1Xch/Rbm24^tm1.1Xch; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB/N

mortality/aging

abnormal survival ( J:259290 )

• unlike Rbm24^tm1.1Xch homozygotes, some mice are viable and exhibit no obvious defects with partial rescue of embryonic lethality

cardiovascular system

cardiovascular system phenotype ( J:259290 )

N • unlike Rbm24^tm1.1Xch homozygotes, some mice are viable and exhibit no obvious defects with normal endocardial cushions with rescue of cardiac tissue apoptosis

Genotype
MGI:5912344

cx243

• Allelic Composition: Tg(Scgb1a1-rtTA)1Jaw/0; Tg(tetO-Kras2)12Hev/0; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB/N

neoplasm

increased lung tumor incidence ( J:73468 )

• doxycycline-treated mice initiate lung tumors more rapidly than in Tg(Scgb1a1-rtTA)1Jaw Tg(tetO-Kras2)12Hev mice with a more malignant phenotype

increased lung adenocarcinoma incidence ( J:73468 )

• more sooner in doxycycline-treated mice compared with Tg(Scgb1a1-rtTA)1Jaw Tg(tetO-Kras2)12Hev mice

respiratory system

increased lung tumor incidence ( J:73468 )

• doxycycline-treated mice initiate lung tumors more rapidly than in Tg(Scgb1a1-rtTA)1Jaw Tg(tetO-Kras2)12Hev mice with a more malignant phenotype

increased lung adenocarcinoma incidence ( J:73468 )

• more sooner in doxycycline-treated mice compared with Tg(Scgb1a1-rtTA)1Jaw Tg(tetO-Kras2)12Hev mice

Genotype
MGI:6152436

cx244

• Allelic Composition: Rbm24^tm1.1Xch/Rbm24^tm1.1Xch; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB/N

cardiovascular system

cardiovascular system phenotype ( J:259290 )

N • unlike Rbm24^tm1.1Xch homozygotes, mice exhibit normal endocardial cushions with rescue of cardiac tissue apoptosis

growth/size/body

fetal growth retardation ( J:259290 )

• at E18.5

Genotype
MGI:5448647

cx245

• Allelic Composition: Nabp2^tm1.2Nfel/Nabp2^tm1.2Nfel; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * FVB/N * SJL

mortality/aging

mortality/aging ( J:190019 )

N • mice are viable and birth and survive up to 24 hours

postnatal lethality, complete penetrance ( J:190019 )

• mice die after 24 hours of birth

skeleton

abnormal cranium morphology ( J:190019 )

abnormal thoracic cage morphology ( J:190019 )

• thoracic rib cage defects are partially rescued

craniofacial

abnormal cranium morphology ( J:190019 )

cleft palate ( J:190019 )

limbs/digits/tail

abnormal limb development ( J:190019 )

• fore- and hindlimb defects are partially rescued

digestive/alimentary system

cleft palate ( J:190019 )

growth/size/body

cleft palate ( J:190019 )

Genotype
MGI:2665138

cx246

• Allelic Composition: Prkdc^scid/Prkdc⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

mortality/aging

premature death ( J:47667 )

• survival time at which half of the mutants are sacrificed or die due to illness is 183 days

neoplasm

increased thymoma incidence ( J:47667 )

• 60% incidence of thymoma

Genotype
MGI:7310098

cx247

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Xrcc3^em4Mjn/Xrcc3^em4Mjn
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

mortality/aging

embryonic lethality during organogenesis, incomplete penetrance ( J:320381 )

• some mice are present at E12.5

preweaning lethality, complete penetrance ( J:320381 )

• no mice are present at weaning

Genotype
MGI:7310097

cx248

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺; Xrcc3^em4Mjn/Xrcc3^em4Mjn
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

mortality/aging

embryonic lethality during organogenesis, incomplete penetrance ( J:320381 )

• some mice are present at E12.5

preweaning lethality, complete penetrance ( J:320381 )

• no mice are present at weaning

Genotype
MGI:5898013

cx249

• Allelic Composition: Ino80^tm1.1Schg/Ino80⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:221224 )

• 7 of 20 mice develop thymic lymphomas

neoplasm

increased T cell derived lymphoma incidence ( J:221224 )

• 7 of 20 mice develop thymic lymphomas

decreased lymphoma incidence ( J:221224 )

• lower incidence of lymphomas compared to Trp53^tm1Tyj null mice

increased sarcoma incidence ( J:221224 )

• 10 of 20 mice develop poorly differentiated and highly invasive soft tissue sarcomas

• while double mutants exhibit an altered spectrum of tumors compared to single Trp53^tm1Tyj, tumor incidence and latency are similar to these mice

Genotype
MGI:5140355

cx250

• Allelic Composition: Rpl27a^Sfa/Rpl27a^Sfa; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

mortality/aging

embryonic lethality, complete penetrance ( J:174216 )

Genotype
MGI:4456092

cx251

• Allelic Composition: Prkdc^scid/Prkdc^scid; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

mortality/aging

premature death ( J:47667 )

• survival time at which half of the mutants are sacrificed or die is 214 days

neoplasm

decreased tumor incidence ( J:47667 )

• none of the mutants develop thymomas by 183 days of age

Genotype
MGI:5140354

cx252

• Allelic Composition: Rpl27a^Sfa/Rpl27a⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

pigmentation

pigmentation phenotype ( J:174216 )

N • foot pad hyperpigmentation is not seen unlike in mice wild-type for Trp53

Genotype
MGI:5898012

cx253

• Allelic Composition: Ino80^tm1.1Schg/Ino80^tm1.1Schg; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

mortality/aging

embryonic lethality, incomplete penetrance ( J:221224 )

• loss of Trp53 does not delay embryonic lethality

preweaning lethality, complete penetrance ( J:221224 )

• by P21 no embryos survived

Genotype
MGI:6283345

cx254

• Allelic Composition: Ercc6l^tm1.2Ajlc/Ercc6l⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6J * C57BL/6N * SJL/J

mortality/aging

lethality during fetal growth through weaning, incomplete penetrance ( J:271028 )

♀ • only one female is born out of 7 expected, indicating that the proportion of viable births is further reduced in a Trp53 null background

Genotype
MGI:6283343

cx255

• Allelic Composition: Ercc6l^tm1.2Ajlc/Y; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6J * C57BL/6N * SJL/J

mortality/aging

embryonic lethality, complete penetrance ( J:271028 )

♂ • no viable mice are born, suggesting that p53-dependent apoptosis and senescence are unlikely to be the only drivers of embryonic lethality

embryo

increased embryonic tissue cell apoptosis ( J:271028 )

♂ • at E10.5, embryos show a significant increase in the number of apoptotic cells, as determined by IHC staining for cleaved caspase-3

decreased embryo size ( J:271028 )

♂ • embryos are smaller at E10.5

growth/size/body

decreased embryo size ( J:271028 )

♂ • embryos are smaller at E10.5

cellular

increased embryonic tissue cell apoptosis ( J:271028 )

♂ • at E10.5, embryos show a significant increase in the number of apoptotic cells, as determined by IHC staining for cleaved caspase-3

chromosomal instability ( J:271028 )

♂ • at E10.5, embryos exhibit an increase in the proportion of gamma-H2AX-positive cells relative to wild-type embryos

Genotype
MGI:6283344

cx256

• Allelic Composition: Ercc6l^tm1.2Ajlc/Y; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6J * C57BL/6N * SJL/J

mortality/aging

embryonic lethality, complete penetrance ( J:271028 )

♂ • no viable mice are born

embryo

increased embryonic tissue cell apoptosis ( J:271028 )

♂ • at E10.5, embryos show a significant increase in the number of apoptotic cells, as determined by IHC staining for cleaved caspase-3

cellular

increased embryonic tissue cell apoptosis ( J:271028 )

♂ • at E10.5, embryos show a significant increase in the number of apoptotic cells, as determined by IHC staining for cleaved caspase-3

chromosomal instability ( J:271028 )

♂ • at E10.5, embryos exhibit an increase in the proportion of gamma-H2AX-positive cells relative to wild-type embryos

Genotype
MGI:6315473

cx257

• Allelic Composition: Aktip^{tm1a(EUCOMM)Hmgu}/Aktip^{tm1a(EUCOMM)Hmgu}; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6N
• Cell Lines: HEPD0589_6_H06

reproductive system

reproductive system phenotype ( J:276210 )

N • male fertility observed in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes is rescued

immune system

peritoneal inflammation ( J:276210 )

• in most mice, more so than in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes

liver inflammation ( J:276210 )

• in most mice, more so than in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes

kidney inflammation ( J:276210 )

• in most mice, more so than in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes

lung inflammation ( J:276210 )

• in most mice, more so than in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes

neoplasm

increased lymphoma incidence ( J:276210 )

• multiorgan in half of mice, single organ in the other half

growth/size/body

decreased body weight ( J:276210 )

• after 31 weeks of age but less than in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes

• however, weight up to 24th week is normal

liver/biliary system

liver inflammation ( J:276210 )

• in most mice, more so than in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes

digestive/alimentary system

peritoneal inflammation ( J:276210 )

• in most mice, more so than in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes

renal/urinary system

kidney inflammation ( J:276210 )

• in most mice, more so than in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes

respiratory system

lung inflammation ( J:276210 )

• in most mice, more so than in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes

skeleton

abnormal bone marrow cavity morphology ( J:276210 )

• bone marrow aplasia in most mice, more so than in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes

Genotype
MGI:5707901

cx258

• Allelic Composition: Rps27l^{Gt(IST11658B7)Tigm}/Rps27l^{Gt(IST11658B7)Tigm}; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6N

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:223276 )

• 7 of 14 mice develop T-lymphoblastic lymphoma

• 1 of 14 mice develop T-cell lymphoma in thymus, lymph node and spleen

mortality/aging

mortality/aging ( J:223276 )

N • postnatal lethality observed in Rps27l^{Gt(IST11658B7)Tigm} homozygotes is rescued

premature death ( J:223276 )

• mice die sooner than mice with a wild-type allele of Rps271

neoplasm

increased T cell derived lymphoma incidence ( J:223276 )

• 7 of 14 mice develop T-lymphoblastic lymphoma

• 1 of 14 mice develop T-cell lymphoma in thymus, lymph node and spleen

increased B cell derived lymphoma incidence ( J:223276 )

• in 1 of 14 mice

hematopoietic system

enlarged spleen ( J:223276 )

decreased bone marrow cell number ( J:223276 )

• partially rescued

cellular

aneuploidy ( J:223276 )

• in lymphoma cells and mouse embryonic fibroblasts

chromosomal instability ( J:223276 )

growth/size/body

growth/size/body region phenotype ( J:223276 )

N • growth retardation and organ hypocellularity (spleen, thymus and bone marrow) observed in Rps27l^{Gt(IST11658B7)Tigm} homozygotes is rescued

enlarged liver ( J:223276 )

enlarged spleen ( J:223276 )

immune system

enlarged spleen ( J:223276 )

enlarged lymph nodes ( J:223276 )

• in 1 of 14 mice

liver/biliary system

enlarged liver ( J:223276 )

Genotype
MGI:5707900

cx259

• Allelic Composition: Rps27l^{Gt(IST11658B7)Tigm}/Rps27l^{Gt(IST11658B7)Tigm}; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6N

mortality/aging

mortality/aging ( J:223276 )

N • postnatal lethality observed in Rps27l^{Gt(IST11658B7)Tigm} homozygotes is rescued

neoplasm

increased lymphoma incidence ( J:223276 )

• 50% of mice are dying of lymphoma by 150 days as in Trp53^tm1Tyj homozygotes

growth/size/body

growth/size/body region phenotype ( J:223276 )

N • growth retardation and organ hypocellularity (spleen, thymus and bone marrow) observed in Rps27l^{Gt(IST11658B7)Tigm} homozygotes is rescued

hematopoietic system

hematopoietic system phenotype ( J:223276 )

N • hematopoietic stem cell depletion and hematopoietic failure observed in Rps27l^{Gt(IST11658B7)Tigm} homozygotes is rescued

Genotype
MGI:6315472

cx260

• Allelic Composition: Aktip^{tm1a(EUCOMM)Hmgu}/Aktip^{tm1a(EUCOMM)Hmgu}; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6N
• Cell Lines: HEPD0589_6_H06

mortality/aging

premature death ( J:276210 )

• more so than in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes with all mice dead before 55 weeks of age

reproductive system

reproductive system phenotype ( J:276210 )

N • male fertility observed in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes is rescued

cellular

cellular phenotype ( J:276210 )

N • mouse embryonic fibroblast do not exhibit increased sensitivity to bleomycin or hydroxyurea unlike cells from Aktip^{tm1a(EUCOMM)Hmgu} homozygotes

increased fibroblast proliferation ( J:276210 )

• in mouse embryonic fibroblasts

neoplasm

increased lymphoma incidence ( J:276210 )

• multiorgan in all mice

growth/size/body

decreased body weight ( J:276210 )

• after 31 weeks of age but less than in Aktip^{tm1a(EUCOMM)Hmgu} homozygotes

• however, weight up to 24th week is normal

Genotype
MGI:6829612

cx261

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺; Tg(Ins2-Mirc13)E4Biat/0
• Genetic Background: involves: 129S2/SvPas * C57BL/6N

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:314874 )

N • mice exhibit normal glucose serum levels unlike mice expressing the transgene alone

Genotype
MGI:7517192

cx262

• Allelic Composition: Trp53^tm1Tyj/Trp53⁺; Zfp871^{tm1a(EUCOMM)Wtsi}/Zfp871^{tm1a(EUCOMM)Wtsi}
• Genetic Background: involves: 129S2/SvPas * C57BL/6N

growth/size/body

decreased birth body size ( J:317166 )

• pups are about half the size of heterozygous littermates

mortality/aging

postnatal lethality, complete penetrance ( J:317166 )

• 3 pups were born alive, out of 33 pups in seven litters, but two died 1 day after birth and the third died at P24

Genotype
MGI:6712735

cx263

• Allelic Composition: Trp53^tm1Tyj/Trp53^tm1Tyj; Commd10^{Tg(Vav1-icre)A2Kio}/Commd10⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6N * C57BL/10 * CBA/Ca

immune system

abnormal interleukin secretion ( J:305794 )

• naive T cells polarized toward the TH22 cell lineage show a decrease in IL-22 secretion

Genotype
MGI:3690112

cx264

• Allelic Composition: Pax3^Sp/Pax3^Sp; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL * C57BL/6J * FVB

nervous system

nervous system phenotype ( J:75569 )

N • all mice have closed neural tubes and no neuroepithelial apoptosis is seen, unlike mice homozygous for the Pax3 mutation alone

Genotype
MGI:3690111

cx265

• Allelic Composition: Pax3^Sp/Pax3^Sp; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * C57BL * C57BL/6J * FVB

nervous system

open neural tube ( J:75569 )

• incidence is reduced to 58% compared to 100% in mice homozygous for the Pax3 mutation alone

embryo

open neural tube ( J:75569 )

• incidence is reduced to 58% compared to 100% in mice homozygous for the Pax3 mutation alone

Genotype
MGI:4819639

cx266

• Allelic Composition: Tg(TRP53)4Dgj/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * FVB

neoplasm

decreased lymphoma incidence ( J:162466 )

• development of early lymphomas in Trp53^tm1Tyj homozygotes is rescued

increased osteosarcoma incidence ( J:162466 )

• more common than in Tg(TRP53*R72P)7Dgj mice

cellular

increased cellular sensitivity to ultraviolet irradiation ( J:162466 )

• UV-exposed mice exhibit increased apoptosis in the skin compared with similarly treated Tg(TRP53*R72P)7Dgj mice

skeleton

increased osteosarcoma incidence ( J:162466 )

• more common than in Tg(TRP53*R72P)7Dgj mice

Genotype
MGI:4819640

cx267

• Allelic Composition: Tg(TRP53*R72P)7Dgj/0; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * FVB

neoplasm

decreased lymphoma incidence ( J:162466 )

• development of early lymphomas in Trp53^tm1Tyj homozygotes is rescued

increased hemangiosarcoma incidence ( J:162466 )

• more common than in Tg(TRP53)4Dgj mice

cellular

decreased cellular sensitivity to ultraviolet irradiation ( J:162466 )

• UV-exposed mice exhibit increased apoptosis in the skin compared with similarly treated Tg(TRP53)4Dgj mice

Genotype
MGI:3836158

cx268

• Allelic Composition: Tg(MMTV-AURKA)#Cxd/?; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S2/SvPas * FVB/N

neoplasm

increased mammary adenocarcinoma incidence ( J:145680 )

• mammary tumors start to develop at 6 months of age

• 70% of mice have developed tumors by 18 months of age

cellular

polyploidy ( J:145680 )

• 25% of mammary epithelial cells from 4-month old mice are polyploidy and show premature chromatid segregation

• about half of mammary epithelial tumor cells are polyploidy

endocrine/exocrine glands

abnormal mammary gland epithelium morphology ( J:145680 )

♀ • 10% of mammary epithelial cells from 4-month old mice contain more than 2 centrosomes per nucleus compared to about 1% mammary epithelial cells from control mice

abnormal branching of the mammary ductal tree ( J:145680 )

♀ • parous mice over one year in age have more extensive ductal branching than transgenic mice not carrying a mutant Trp53 allele

mammary gland duct hyperplasia ( J:145680 )

♀ • parous mice have almost 6-fold more actively proliferating cells in the mammary epithelium than in controls

increased mammary adenocarcinoma incidence ( J:145680 )

• mammary tumors start to develop at 6 months of age

• 70% of mice have developed tumors by 18 months of age

integument

abnormal mammary gland epithelium morphology ( J:145680 )

♀ • 10% of mammary epithelial cells from 4-month old mice contain more than 2 centrosomes per nucleus compared to about 1% mammary epithelial cells from control mice

abnormal branching of the mammary ductal tree ( J:145680 )

♀ • parous mice over one year in age have more extensive ductal branching than transgenic mice not carrying a mutant Trp53 allele

mammary gland duct hyperplasia ( J:145680 )

♀ • parous mice have almost 6-fold more actively proliferating cells in the mammary epithelium than in controls

increased mammary adenocarcinoma incidence ( J:145680 )

• mammary tumors start to develop at 6 months of age

• 70% of mice have developed tumors by 18 months of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
breast cancer		DOID:1612	OMIM:114480	J:145680

Genotype
MGI:5568940

cx269

• Allelic Composition: Pip4k2a^tm1.2Lca/Pip4k2a^tm1.2Lca; Pip4k2b^{Gt(Betageo)1Lca}/Pip4k2b⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S/SvEv * 129S2/SvPas * 129S5/SvEvBrd

neoplasm

decreased tumor incidence ( J:205288 )

• mice show a dramatic reduction in tumor formation and increased survival compared to single Trp53 homozygotes

Genotype
MGI:4462851

cx270

• Allelic Composition: Ssbp2^tm1Lana/Ssbp2^tm1Lana; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S/SvEv * 129S2/SvPas * BALB/c * C57BL/6

mortality/aging

premature death ( J:162035 )

• median survival is 122 days instead of 182 days for Trp53^tm1Tyj homozygotes

neoplasm

increased T cell derived lymphoma incidence ( J:162035 )

• mice exhibit a 2.4-fold increase in thymic lymphomas compared with Trp53^tm1Tyj homozygotes

• thymic lymphomas are more aggressive than in Trp53^tm1Tyj homozygotes

immune system

thymus hypoplasia ( J:162035 )

• at 3 and 6 months

hematopoietic system

thymus hypoplasia ( J:162035 )

• at 3 and 6 months

endocrine/exocrine glands

thymus hypoplasia ( J:162035 )

• at 3 and 6 months

increased T cell derived lymphoma incidence ( J:162035 )

• mice exhibit a 2.4-fold increase in thymic lymphomas compared with Trp53^tm1Tyj homozygotes

• thymic lymphomas are more aggressive than in Trp53^tm1Tyj homozygotes

Genotype
MGI:2177218

cx271

• Allelic Composition: Brca2^tm1Arge/Brca2^tm1Arge; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S/SvEv * 129S2/SvPas * C57BL/6

mortality/aging

prenatal lethality ( J:40594 )

embryo

abnormal embryonic tissue morphology ( J:40594 )

• Trp53 deficiency appears to partially rescue the Brca2 homozygous phenotype in that some appear similar to wild-type and others are similar to or more advanced that the most advanced Brca2 single homozygous embryos

nervous system

exencephaly ( J:40594 )

Genotype
MGI:3580070

cx272

• Allelic Composition: Nf1^tm1Fcr/Nf1⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S/SvEv * 129S2/SvPas * C57BL/6

mortality/aging

postnatal lethality, incomplete penetrance ( J:58877 )

• die as early as 3 weeks of age

neoplasm

increased lymphoma incidence ( J:58877 )

• develop tumors, primarily lymphomas

Genotype
MGI:3580069

cx273

• Allelic Composition: Nf1^tm1Fcr/Nf1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129S/SvEv * 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:58877 )

• cis-double heterozygotes died at 15 weeks and trans-double heterozygotes died at 25 weeks

neoplasm

increased fibrohistocytoma incidence ( J:58877 )

• developed in cis-double heterozygotes

increased lymphoma incidence ( J:58877 )

• developed in cis-double heterozygotes

increased neuroblastoma incidence ( J:58877 )

• developed in cis-double heterozygotes

increased carcinoma incidence ( J:58877 )

• developed in cis-double heterozygotes

increased malignant triton tumor incidence ( J:58877 )

• developed in cis-double heterozygotes

increased sarcoma incidence ( J:58877 )

• both cis- and trans-double heterozygotes developed sarcomas

increased leiomyosarcoma incidence ( J:58877 )

• developed in cis-double heterozygotes

increased rhabdomyosarcoma incidence ( J:58877 )

• developed in cis-double heterozygotes

increased neurofibrosarcoma incidence ( J:58877 )

• developed in cis-double heterozygotes

integument

increased fibrohistocytoma incidence ( J:58877 )

• developed in cis-double heterozygotes

muscle

increased leiomyosarcoma incidence ( J:58877 )

• developed in cis-double heterozygotes

increased rhabdomyosarcoma incidence ( J:58877 )

• developed in cis-double heterozygotes

nervous system

increased neuroblastoma incidence ( J:58877 )

• developed in cis-double heterozygotes

increased neurofibrosarcoma incidence ( J:58877 )

• developed in cis-double heterozygotes

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
neurofibromatosis 1		DOID:0111253	OMIM:162200	J:58877

Genotype
MGI:2177217

cx274

• Allelic Composition: Brca1^tm1Arge/Brca1^tm1Arge; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S/SvEv * 129S2/SvPas * C57BL/6

mortality/aging

prenatal lethality ( J:40594 )

growth/size/body

embryonic growth retardation ( J:40594 )

• although double homozygous embryos are overtly retarded and abnormal compared to controls, Trp53 deficiency appears to partially rescue the Brca1 homozygous phenotype in that the embryos develop to a more advanced stage

embryo

embryonic growth retardation ( J:40594 )

• although double homozygous embryos are overtly retarded and abnormal compared to controls, Trp53 deficiency appears to partially rescue the Brca1 homozygous phenotype in that the embryos develop to a more advanced stage

Genotype
MGI:2665118

cx275

• Allelic Composition: Rag2^tm1Fwa/Rag2^tm1Fwa; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S/SvEv * 129S2/SvPas * C57BL/6J

mortality/aging

premature death ( J:47667 )

• survival time at which half of the mutants are sacrificed or die due to illness is 180 days

neoplasm

increased T cell derived lymphoma incidence ( J:47667 )

• thymoma develops in 67% of mutants

• tumors arise more slowly or with longer latency than in mice homozygous for Rag2 and heterozygous for Trp53, with mutants living 9% longer than controls

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:47667 )

• thymoma develops in 67% of mutants

• tumors arise more slowly or with longer latency than in mice homozygous for Rag2 and heterozygous for Trp53, with mutants living 9% longer than controls

Genotype
MGI:2665119

cx276

• Allelic Composition: Rag2^tm1Fwa/Rag2⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S/SvEv * 129S2/SvPas * C57BL/6J

mortality/aging

premature death ( J:47667 )

• survival time at which half of the mutants are sacrificed or die due to illness is 165 days

neoplasm

increased T cell derived lymphoma incidence ( J:47667 )

• thymoma develops in 55% of mutants, a lower frequency than in Trp53 homozygous mice

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:47667 )

• thymoma develops in 55% of mutants, a lower frequency than in Trp53 homozygous mice

Genotype
MGI:4839565

cx277

• Allelic Composition: Cdkn2a^tm1.1Brn/Cdkn2a^tm1.1Brn; Pknox1^tm1Fbla/Pknox1^tm1Fbla; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129/Sv * 129P2/OlaHsd * 129S2/SvPas * C57BL/6

mortality/aging

preweaning lethality, complete penetrance ( J:165811 )

• no mice are recovered (no time of death given)

Genotype
MGI:3814379

cx278

• Allelic Composition: Tg(IghMyc)22Bri/0; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129/Sv * 129X1/SvJ * C57BL * C57BL/6 * SJL

mortality/aging

premature death ( J:125164 )

• mice die prior to 20 weeks of age

neoplasm

increased B cell derived lymphoma incidence ( J:125164 )

• mice exhibit an earlier age of onset and enhanced penetrance of B cell lymphomas compared to in Tg(IghMyc)22Bri mice

Genotype
MGI:3033461

cx279

• Allelic Composition: Dph1^tm2Bhr/Dph1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129/Sv * C57BL/6

neoplasm

decreased tumor latency ( J:88090 )

• latency of 52 weeks as opposed to 70 weeks

Genotype
MGI:3033460

cx280

• Allelic Composition: Dph1^tm2Bhr/Dph1^tm2Bhr; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129/Sv * C57BL/6

mortality/aging

neonatal lethality, complete penetrance ( J:88090 )

• homozygotes die soon after birth

embryonic lethality during organogenesis, incomplete penetrance ( J:88090 )

• 30-50% of embryos die between E11.5 and E13.5

cellular

cellular phenotype ( J:88090 )

N • proliferation defect in cultured MEFs rescued by this genotype

Genotype
MGI:3580073

cx281

• Allelic Composition: Nf1^tm1Tyj/Nf1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129/Sv * C57BL/6

mortality/aging

premature death ( J:58876 )

• cis-double heterozygotes die by 5 months of age and trans-double heterozygotes survive to the average age of 10 months

neoplasm

increased tumor incidence ( J:58876 )

• cis-double heterozygotes exhibit greater incidence of tumors than trans-double heterozygotes

increased sarcoma incidence ( J:58876 )

• developed in both cis- and trans-double heterozygotes

• sarcomas in trans-double heterozygotes were similar to those found in mice with either single mutation and were usually correlated with loss of one chromosome

increased neurofibrosarcoma incidence ( J:58876 )

• develop in cis-double heterozygotes, usually correlated with loss of one chromosome

nervous system

increased neurofibrosarcoma incidence ( J:58876 )

• develop in cis-double heterozygotes, usually correlated with loss of one chromosome

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
neurofibromatosis 1		DOID:0111253	OMIM:162200	J:58876

Genotype
MGI:3575575

cx282

• Allelic Composition: Motp1^CE/J/Motp1^CE/J; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: involves: 129-Trp53^tm1Tyj/J * CE/J

mortality/aging

prenatal lethality, incomplete penetrance ( J:97137 )

• increased embryonic lethality

reproductive system

transmission ratio distortion ( J:97137 )

Genotype
MGI:3575574

cx283

• Allelic Composition: Motp1^CE/J/Motp1^CE/J; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129-Trp53^tm1Tyj/J * CE/J

mortality/aging

prenatal lethality, incomplete penetrance ( J:97137 )

• increased embryonic lethality

reproductive system

transmission ratio distortion ( J:97137 )

Genotype
MGI:5606045

cx284

• Allelic Composition: Susd6^tm1.1Geno/Susd6^tm1.1Geno; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: C57BL/6J

mortality/aging

premature death ( J:210814 )

• median survival time of 166 days compared to 190 days in p53^-/- mice

Genotype
MGI:5606044

cx285

• Allelic Composition: Susd6^tm1.1Geno/Susd6⁺; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: C57BL/6J

mortality/aging

premature death ( J:210814 )

• median survival time of 166 days compared to 190 days in p53^-/- mice

Genotype
MGI:5286082

cx286

• Allelic Composition: Nf1^tm1Tyj/Nf1⁺; Trp53^tm1Tyj/Trp53⁺
• Genetic Background: (SJL/J x B6.129S2-Trp53^tm1Tyj Nf1^tm1Tyj/+ +)F1

nervous system

increased glioblastoma incidence ( J:64364 )

increased brain tumor incidence ( J:64364 )

• brain tumors range from diffuse cells with nuclear atypia to glioblastoma multiforme

• Background Sensitivity: mice on a congenic C57BL/6 or C3H/HeJ F1 background develop more brain tumors compared with mice on a CAST/EiJ or SJL/J F1 background

increased astrocytoma incidence ( J:64364 )

mortality/aging

decreased tumor-free survival time ( J:64364 )

• in mice with advanced tumors

neoplasm

increased glioblastoma incidence ( J:64364 )

increased brain tumor incidence ( J:64364 )

• brain tumors range from diffuse cells with nuclear atypia to glioblastoma multiforme

• Background Sensitivity: mice on a congenic C57BL/6 or C3H/HeJ F1 background develop more brain tumors compared with mice on a CAST/EiJ or SJL/J F1 background

increased astrocytoma incidence ( J:64364 )

behavior/neurological

ataxia ( J:64364 )

• in mice with advanced tumors

paralysis ( J:64364 )

• in mice with advanced tumors

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
malignant astrocytoma		DOID:3069		J:64364