Phenotypes associated with this allele

• Allele Symbol: Ctnnb1⁺
• Allele Name: wild type
• Allele ID: MGI:2440294
• Summary: 79 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
ht1	Ctnnb1^Bfc/Ctnnb1^+	either: (involves: BALB/cCrl * C3H/HeNCrl) or (involves: BALB/cCrl * C3H/HeNCrl * C57BL/6)	MGI:4947308
ht2	Ctnnb1^tm1(Nfkbia)Rsu/Ctnnb1^+	involves: 129P2/OlaHsd * C57BL/6	MGI:3706574
ht3	Ctnnb1^tm1.2Wvv/Ctnnb1^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:5430609
ht4	Ctnnb1^tm1Mmt/Ctnnb1^+	involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ	MGI:4943530
ht5	Ctnnb1^tm1Mmt/Ctnnb1^+	involves: 129X1/SvJ	MGI:2673885
ht6	Ctnnb1^Bfc/Ctnnb1^+	involves: BALB/cCrl * C3H/HeNCrl	MGI:2656754
cn7	Ctnnb1^tm2(Nfkbia)Rsu/Ctnnb1^+ Tg(Myh6-cre)2182Mds/0	B6.Cg-Ctnnb1^tm2(Nfkbia)Rsu Tg(Myh6-cre)2182Mds	MGI:3706583
cn8	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Wap-cre)11738Mam/0	FVB.Cg-Ctnnb1^tm1Mmt Tg(Wap-cre)11738Mam	MGI:5576521
cn9	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Wap-cre)11738Mam/0 Tg(Wap-Hgf)402Mig/0	FVB.Cg-Ctnnb1^tm1Mmt Tg(Wap-cre)11738Mam Tg(Wap-Hgf)402Mig	MGI:5576520
cn10	Ctnnb1^tm1Mmt/Ctnnb1^+ Cxcr4^tm2Yzo/Cxcr4^tm2Yzo Tg(Wap-cre)11738Mam/0 Tg(Wap-Hgf)402Mig/0	FVB.Cg-Cxcr4^tm2Yzo Ctnnb1^tm1Mmt Tg(Wap-cre)11738Mam Tg(Wap-Hgf)402Mig	MGI:5576532
cn11	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Msx2-rtTA)885Lma/0 Tg(tetO-cre)1Jaw/0	involves: 129 * 129X1/SvJ * C57BL/6	MGI:5546509
cn12	Ctnnb1^tm2Kem/Ctnnb1^+ Gt(ROSA)26Sor^tm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor^+ Tg(Col2a1-cre)1Bhr/0 Tg(tetO-Vegfa)90Ala/0	involves: 129 * C57BL/6 * FVB/N * ICR * SJL	MGI:4429127
cn13	Ctnnb1^tm2Kem/Ctnnb1^+ Tg(Prrx1-cre)1Cjt/0	involves: 129 * C57BL/6 * SJL	MGI:5086016
cn14	Ctnnb1^tm2Kem/Ctnnb1^+ Amer1^tm1.1Nbar/Y Tg(Prrx1-cre)1Cjt/0	involves: 129 * C57BL/6 * SJL	MGI:5086015
cn15	Ctnnb1^tm4Wbm/Ctnnb1^+ Tg(KRT14-cre)1Efu/0	involves: 129P2/OlaHsd	MGI:5435570
cn16	Ctnnb1^tm2Kem/Ctnnb1^+ Hesx1^tm1(cre)Jpmb/Hesx1^tm1Icar	involves: 129P2/OlaHsd * 129S * 129X1/SvJ * C57BL/6	MGI:5314537
cn17	Ctnnb1^tm2Kem/Ctnnb1^+ Lyz2^tm1(cre)Ifo/Lyz2^+	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ	MGI:5581947
cn18	Ctnnb1^tm2Kem/Ctnnb1^+ Pparg^tm1.1(tTA)Jmgr/Pparg^+ Tg(tetO-cre)1Jaw/0	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:5581952
cn19	Bmpr1a^tm2.1Bhr/Bmpr1a^tm2.1Bhr Ctnnb1^tm1Mmt/Ctnnb1^+ Krt14^tm1.1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * 129S7/SvEvBrd * 129X1/SvJ	MGI:5508218
cn20	Ctnnb1^tm1Mmt/Ctnnb1^+ Krt14^tm1.1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * 129X1/SvJ	MGI:5508224
cn21	Ctnnb1^tm1Mmt/Ctnnb1^+ Lgr5^tm1(cre/ERT2)Cle/Lgr5^+	involves: 129P2/OlaHsd * 129X1/SvJ	MGI:5475209
cn22	Ctnnb1^tm1Mmt/Ctnnb1^+ Lyz2^tm1(cre)Ifo/Lyz2^+	involves: 129P2/OlaHsd * 129X1/SvJ	MGI:5581954
cn23	Ctnnb1^tm1Mmt/Ctnnb1^+ Pparg^tm1.1(tTA)Jmgr/Pparg^+ Tg(tetO-cre)1Jaw/0	involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6	MGI:5581956
cn24	Ctnnb1^tm1Mmt/Ctnnb1^+ Sox2^tm1.1(cre/ERT2)Jpmb/Sox2^+	involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6	MGI:5512969
cn25	Ctnnb1^tm1Mmt/Ctnnb1^+ Pik3ca^tm1Gilb/Pik3ca^+ Trp53^tm1Brn/Trp53^+ Tg(Fabp7-cre,-lacZ)3Gtm/0	involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * CBA	MGI:5438217
cn26	Ctnnb1^tm1Mmt/Ctnnb1^+ Trp53^tm1Brn/Trp53^+ Tg(Fabp7-cre,-lacZ)3Gtm/0	involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * CBA	MGI:5438218
cn27	Ctnnb1^tm2(Nfkbia)Rsu/Ctnnb1^+ Tg(CMV-cre)1Cgn/0	involves: 129P2/OlaHsd * BALB/cJ * C57BL/6	MGI:3706580
cn28	Apc^tm1Rsmi/Apc^+ Ctnnb1^tm1Wvv/Ctnnb1^+ Tg(Fabp1-cre)1Jig/?	involves: 129P2/OlaHsd * C57BL/6J * FVB/N	MGI:5430612
cn29	Ctnnb1^tm2Kem/Ctnnb1^+ Pten^tm1Hwu/Pten^tm1Hwu Tg(Cdh5-cre)7Mlia/0	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * BALB/c * C57BL/6 * FVB/N	MGI:4839562
cn30	Bmi1^tm1(cre/ERT)Mrc/Bmi1^+ Ctnnb1^tm1Mmt/Ctnnb1^+	involves: 129S1/Sv * 129X1/SvJ	MGI:3805821
cn31	Ctnnb1^tm2Kem/Ctnnb1^+ Osr2^tm2(cre)Jian/Osr2^+	involves: 129S1/Sv * 129X1/SvJ	MGI:4365782
cn32	Ctnnb1^tm1Mmt/Ctnnb1^+ Kras^tm1Bbd/Kras^+ Tg(Pbsn-cre)4Prb/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2	MGI:3836578
cn33	Ctnnb1^tm1Mmt/Ctnnb1^+ Igs2^tm1(CAG-Met)Zsu/Igs2^+ Tg(Pbsn-cre)4Prb/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 * FVB/N	MGI:6507888
cn34	Ctnnb1^tm2Kem/Ctnnb1^+ Nanos3^tm2(cre)Ysa/Nanos3^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6NCrlj * CBA/JNCrlj	MGI:6358667
cn35	Ctnnb1^tm2Kem/Ctnnb1^+ Ctsk^tm1(cre)Ska/Ctsk^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6NCrlj * CBA/JNCrlj	MGI:5581945
cn36	Ctnnb1^tm2Kem/Ctnnb1^+ Tg(Tek-cre)1Ywa/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:5581948
cn37	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Mx1-cre)1Cgn/0	involves: 129S1/Sv * C57BL/6 * CBA	MGI:3701505
cn38	Amhr2^tm3(cre)Bhr/Amhr2^+ Ctnnb1^tm1Mmt/Ctnnb1^+ Pten^tm1Hwu/Pten^tm1Hwu	involves: 129S4/SvJae * 129S7/SvEvBrd * 129X1/SvJ	MGI:4941746
cn39	Ctnnb1^tm1Mmt/Ctnnb1^+ Kras^tm4Tyj/Kras^+ Amhr2^tm3(cre)Bhr/Amhr2^+	involves: 129S4/SvJae * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6	MGI:5432231
cn40	Amhr2^tm3(cre)Bhr/Amhr2^+ Ctnnb1^tm1Mmt/Ctnnb1^+ Pten^tm1Hwu/Pten^tm1Hwu	involves: 129S4/SvJae * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6	MGI:5432232
cn41	Ctnnb1^tm1Mmt/Ctnnb1^+ Kras^tm4Tyj/Kras^+ Tg(CYP19A1-cre)1Jri/0	involves: 129S4/SvJae * 129X1/SvJ * C57BL/6	MGI:5432224
cn42	Ctnnb1^tm1Mmt/Ctnnb1^+ Pten^tm1Hwu/Pten^tm1Hwu Tg(CYP19A1-cre)1Jri/0	involves: 129S4/SvJae * 129X1/SvJ * C57BL/6	MGI:5432226
cn43	Ctnnb1^tm1Mmt/Ctnnb1^+ Kras^tm4Tyj/Kras^+ Tg(Upk2-cre)6Xrw/0	involves: 129S4/SvJae * 129X1/SvJ * FVB/N	MGI:5141743
cn44	Ctnnb1^tm1Mmt/Ctnnb1^+ Pten^tm1Hwu/Pten^tm1Hwu Tg(Upk2-cre)6Xrw/0	involves: 129S4/SvJae * 129X1/SvJ * FVB/N	MGI:4943270
cn45	Ctnnb1^tm1Mmt/Ctnnb1^+ Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Prom1^tm1(cre/ERT2)Gilb/Prom1^+	involves: 129S6/SvEvTac * 129X1/SvJ	MGI:3830626
cn46	Ctnnb1^tm1Mmt/Ctnnb1^+ Fgfr3^tm4Cxd/Fgfr3^+ Tg(Upk2-cre)6Xrw/0	involves: 129S6/SvEvTac * 129X1/SvJ * FVB/N	MGI:5141741
cn47	Amhr2^tm3(cre)Bhr/Amhr2^+ Ctnnb1^tm1Mmt/Ctnnb1^+	involves: 129S7/SvEvBrd * 129X1/SvJ * C57BL/6	MGI:5432228
cn48	Ctnnb1^tm1Mmt/Ctnnb1^+ Rspo1^tm1Mcch/Rspo1^tm1Mcch Tg(Nr5a1-cre)5Asc/?	involves: 129/Sv * C57BL/6 * CBA	MGI:3795284
cn49	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Pou3f4-cre)32Cren/?	involves: 129X1/SvJ	MGI:2673253
cn50	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Col2a1-cre)1Bhr/0	involves: 129X1/SvJ	MGI:3045411
cn51	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Fabp1-cre)1Mmt/?	involves: 129X1/SvJ	MGI:2673888
cn52	Ctnnb1^tm1Mmt/Ctnnb1^+ Krt19^tm1(cre)Mmt/Krt19^+	involves: 129X1/SvJ	MGI:2673257
cn53	Ctnnb1^tm1Mmt/Ctnnb1^+ Dclk1^tm1.1(cre/ERT2)Seno/Dclk1^+	involves: 129X1/SvJ * C57BL/6	MGI:5475208
cn54	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Tcfap2a-cre)1Will/0	involves: 129X1/SvJ * C57BL/6	MGI:4887452
cn55	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(CYP19A1-cre)1Jri/0	involves: 129X1/SvJ * C57BL/6	MGI:5432223
cn56	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Hoxb7-cre)13Amc/0	involves: 129X1/SvJ * C57BL/6	MGI:5289781
cn57	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Pbsn-cre)4Prb/0	involves: 129X1/SvJ * C57BL/6 * DBA/2	MGI:3836579
cn58	Ctnnb1^tm1Mmt/Ctnnb1^+ Nanos3^tm2(cre)Ysa/Nanos3^+	involves: 129X1/SvJ * C57BL/6J * C57BL/6NCrlj * CBA/JNCrlj	MGI:6358659
cn59	Ctnnb1^tm1Mmt/Ctnnb1^+ Ctsk^tm1(cre)Ska/Ctsk^+	involves: 129X1/SvJ * C57BL/6NCrlj * CBA/JNCrlj	MGI:5581953
cn60	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Tek-cre)1Ywa/0	involves: 129X1/SvJ * C57BL/6 * SJL	MGI:5581955
cn61	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0	involves: 129X1/SvJ * CD-1	MGI:3689416
cn62	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Col1a1-cre)1Kry/0	involves: 129X1/SvJ * FVB	MGI:5319652
cn63	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Upk2-cre)6Xrw/0	involves: 129X1/SvJ * FVB/N	MGI:4943264
cn64	Ctnnb1^tm1Mmt/Ctnnb1^+ Tg(Cdh16-cre)91Igr/0	involves: 129X1/SvJ * ICR	MGI:5428002
cn65	Ctnnb1^tm1Mmt/Ctnnb1^+ Wnt9b^tm1.1Amc/Wnt9b^tm1.2Amc Tg(Cdh16-cre)91Igr/0	involves: 129X1/SvJ * ICR	MGI:5428001
cx66	Ctnnb1^Bfc/Ctnnb1^+ Dkk1^tm1Lmgd/Dkk1^+ Lrp6^Gw/Lrp6^+	either: (involves: 101/H * 129 * BALB/cCrl * C3H) or (involves: 101/H * 129 * BALB/cCrl * C3H * C57BL/6)	MGI:4947311
cx67	Ctnnb1^Bfc/Ctnnb1^+ Lrp6^Gw/Lrp6^+	either: (involves: 101/H * BALB/cCrl * C3H) or (involves: 101/H * BALB/cCrl * C3H * C57BL/6)	MGI:4947310
cx68	Ctnnb1^Bfc/Ctnnb1^+ Dkk1^tm1Lmgd/Dkk1^+	either: (involves: 129/Sv * BALB/cCrl * C3H/HeNCrl) or (involves: 129/Sv * BALB/cCrl * C3H/HeNCrl * C57BL/6)	MGI:4947312
cx69	Apc^tm1Tno/Apc^tm1Tno Ctnnb1^tm4.1Wbm/Ctnnb1^+	involves: 129 * 129P2/OlaHsd * 129S4/SvJae * C57BL/6	MGI:4429576
cx70	Apc^Min/Apc^tm1Tno Ctnnb1^tm4.1Wbm/Ctnnb1^+	involves: 129 * 129P2/OlaHsd * 129S4/SvJae * C57BL/6	MGI:4429574
cx71	Apc^Min/Apc^Min Ctnnb1^tm4.1Wbm/Ctnnb1^+	involves: 129 * 129P2/OlaHsd * C57BL/6	MGI:4429575
cx72	Ctnnb1^tm1Max/Ctnnb1^+ Hesx1^tm1(cre)Jpmb/Hesx1^tm1Icar	involves: 129P2/OlaHsd * 129S * 129X1/SvJ * C57BL/6	MGI:5314535
cx73	Ctnnb1^tm1Max/Ctnnb1^+ Hesx1^tm1Icar/Hesx1^tm1Icar	involves: 129P2/OlaHsd * 129S * 129X1/SvJ * C57BL/6	MGI:5314538
cx74	Ctnnb1^tm1Mmt/Ctnnb1^+ Tcf7^tm1Cle/Tcf7^+	involves: 129P2/OlaHsd * 129X1/SvJ	MGI:5319651
cx75	Apc^tm2Rfo/Apc^+ Ctnnb1^tm1.2Wvv/Ctnnb1^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:5430611
cx76	Apc^tm1Rak/Apc^+ Ctnnb1^tm1.2Wvv/Ctnnb1^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:5430610
cx77	Ctnnb1^tm2.1Kem/Ctnnb1^+ Sall4^Gt(W097E01)Flo/Sall4^+	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6	MGI:3809920
cx78	Axin1^tm4Cos/Axin1^tm4Cos Ctnnb1^tm2.1Kem/Ctnnb1^+	involves: 129S1/Sv * 129X1/SvJ * FVB/N	MGI:3840269
cx79	Ctnnb1^tm2.1Kem/Ctnnb1^+ Otx2^tm1(Dkk1)Imat/Otx2^tm1(Dkk1)Imat	involves: 129/Sv * C57BL/6 * CBA	MGI:3612484

Genotype
MGI:4947308

ht1

• Allelic Composition: Ctnnb1^Bfc/Ctnnb1⁺
• Genetic Background: either: (involves: BALB/cCrl * C3H/HeNCrl) or (involves: BALB/cCrl * C3H/HeNCrl * C57BL/6)

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

mortality/aging

preweaning lethality, incomplete penetrance ( J:170646 )

• fewer than expected mice are produced

vision/eye

abnormal eye morphology ( J:170646 )

• mice exhibit ocular defects that are more prominent on a background with C57BL/6 compared with BALB/c

cataract ( J:170646 )

• mice exhibit cataract-like lens opacity unlike wild-type mice

microphthalmia ( J:170646 )

anophthalmia ( J:170646 )

nervous system

forebrain hypoplasia ( J:170646 )

• 38% of mice at E8-9.0 and 90% of mice at E9-10 exhibit head defects with reduced forebrain unlike wild-type mice

craniofacial

flattened snout ( J:170646 )

• squashed snout

growth/size/body

abnormal head morphology ( J:170646 )

• 38% of mice at E8-9.0 and 90% of mice at E9-10 exhibit head defects with reduced forebrain unlike wild-type mice

• 23% of mice exhibit reduced head tissue compared with wild-type mice

• at E9.0 to E10.0, 27% of mice exhibit head defects compared with 2% of wild-type mice

flattened snout ( J:170646 )

• squashed snout

Genotype
MGI:3706574

ht2

• Allelic Composition: Ctnnb1^{tm1(Nfkbia)Rsu}/Ctnnb1⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

mortality/aging

premature death ( J:71744 )

• 50% of mutants live less than 6 months

• the maximum life span is 1 year

prenatal lethality, incomplete penetrance ( J:71744 )

• a proportion of mutants die during embryogenesis

immune system

increased leukocyte cell number ( J:71744 )

increased granulocyte number ( J:71744 )

• granulocytosis

abnormal macrophage physiology ( J:71744 )

• impaired macrophage activity

decreased Peyer's patch number ( J:71744 )

• Peyer's patches are reduced in size and numbers in 90% of mutants

small Peyer's patches ( J:71744 )

absent Peyer's patches ( J:71744 )

• Peyer's patches are absent in 10% of mutants

abnormal peripheral lymph node morphology ( J:71744 )

small axillary lymph nodes ( J:71744 )

• mutants posses only small numbers of minute axilar/brachial lymph nodes

small brachial lymph nodes ( J:71744 )

• mutants posses only small numbers of minute axilar/brachial lymph nodes

abnormal cervical lymph node morphology ( J:71744 )

• mutants have only small numbers of superficial cervical lymph nodes

absent popliteal lymph nodes ( J:71744 )

• absent draining popliteal lymph nodes

absent peripheral lymph nodes ( J:71744 )

• absent peripheral lymph nodes

increased inflammatory response ( J:71744 )

increased susceptibility to otitis media ( J:71744 )

• middle ear exhibits chronic otitis media

conjunctivitis ( J:71744 )

• after about 1 month, mutants develop conjunctivitis

keratoconjunctivitis sicca ( J:71744 )

• mutants acquire severe keratoconjunctivits sicca, due to a reduced immune response, eventually resulting in blindness

increased susceptibility to parasitic infection ( J:71744 )

• mutants infected with Leishmania major develop significantly more severe lesions than wild-type; increased infection susceptibility is caused by reduced NOS2 activity in macrophages and not by type I T-helper-cell deficiencies

vision/eye

conjunctivitis ( J:71744 )

• after about 1 month, mutants develop conjunctivitis

keratoconjunctivitis sicca ( J:71744 )

• mutants acquire severe keratoconjunctivits sicca, due to a reduced immune response, eventually resulting in blindness

abnormal eye morphology ( J:71744 )

• mutants reaching adulthood have slanted eyes

absent Meibomian glands ( J:71744 )

abnormal cornea epithelium morphology ( J:71744 )

• keratinization of the corneal epithelium is seen after 6 months of age

abnormal cornea stroma morphology ( J:71744 )

• hyperproliferation of the corneal stroma is detected after 6 months of age

narrow eye opening ( J:71744 )

• palpebral fissures are narrowed

abnormal eyelid margin morphology ( J:71744 )

• margins of the eyelids are thickened, caused by a hyperproliferative epidermis of the eyelid margin

early eyelid opening ( J:71744 )

• eyes open only after 2.5-3 weeks after birth

• however, the eye-bulb, conjunctiva, and the cornea develop normally

blindness ( J:71744 )

• blindness occurs as a result of severe keratoconjunctivitis sicca

dry eyes ( J:71744 )

• the eyes dehydrate with time due to the absence of the Meibomian glands

growth/size/body

misaligned incisors ( J:71744 )

• abnormal incisor positioning

short incisors ( J:71744 )

• incisors do not reach normal lengths in adults

small molars ( J:71744 )

• molars do not reach normal lengths in adults

growth retardation of incisors ( J:71744 )

• outgrowth of incisors is delayed

growth retardation of molars ( J:71744 )

• outgrowth of molars is delayed

decreased body size ( J:71744 )

• mutants reaching adulthood are small and thin, about 50-70% of wild-type

endocrine/exocrine glands

absent Meibomian glands ( J:71744 )

Harderian gland atrophy ( J:71744 )

• atrophy of Harderian glands

abnormal sweat gland morphology ( J:71744 )

• the sweat glands are absent in the foot pads

hearing/vestibular/ear

deafness ( J:71744 )

• hearing tests reveal deafness starting at 4-6 weeks of age

increased susceptibility to otitis media ( J:71744 )

• middle ear exhibits chronic otitis media

digestive/alimentary system

gastrointestinal hemorrhage ( J:71744 )

• lethal bleedings in the gut

abnormal intestinal goblet cell morphology ( J:71744 )

• reduction in the number of intestinal goblet cells

abnormal small intestine morphology ( J:71744 )

• the epithelial structure of the small intestine is loosened

cardiovascular system

gastrointestinal hemorrhage ( J:71744 )

• lethal bleedings in the gut

liver hemorrhage ( J:71744 )

• lethal bleedings in the liver

craniofacial

misaligned incisors ( J:71744 )

• abnormal incisor positioning

short incisors ( J:71744 )

• incisors do not reach normal lengths in adults

small molars ( J:71744 )

• molars do not reach normal lengths in adults

growth retardation of incisors ( J:71744 )

• outgrowth of incisors is delayed

growth retardation of molars ( J:71744 )

• outgrowth of molars is delayed

domed cranium ( J:71744 )

hematopoietic system

increased leukocyte cell number ( J:71744 )

increased granulocyte number ( J:71744 )

• granulocytosis

abnormal macrophage physiology ( J:71744 )

• impaired macrophage activity

homeostasis/metabolism

abnormal nitric oxide homeostasis ( J:71744 )

• reduced nitric oxide production

liver/biliary system

liver hemorrhage ( J:71744 )

• lethal bleedings in the liver

increased hepatocyte apoptosis ( J:71744 )

• livers show an increase in embryonic (E12.5-14.5) hepatocyte apoptosis

• however, mutants surviving to birth and adulthood, do not show gross liver abnormalities

reproductive system

decreased litter size ( J:71744 )

skeleton

misaligned incisors ( J:71744 )

• abnormal incisor positioning

short incisors ( J:71744 )

• incisors do not reach normal lengths in adults

small molars ( J:71744 )

• molars do not reach normal lengths in adults

growth retardation of incisors ( J:71744 )

• outgrowth of incisors is delayed

growth retardation of molars ( J:71744 )

• outgrowth of molars is delayed

domed cranium ( J:71744 )

limbs/digits/tail

abnormal foot pad morphology ( J:71744 )

• in the foot pads, plicae digitalis (deeply indented transversed folds) and sweat glands are absent

kinked tail ( J:71744 )

behavior/neurological

lethargy ( J:71744 )

tremors ( J:71744 )

impaired balance ( J:71744 )

• mutants show equilibrium problems

• however, the inner ear structure and hair cells show no abnormalities

hunched posture ( J:71744 )

integument

increased hair follicle apoptosis ( J:71744 )

• mutants exhibit an increased rate of apoptosis in many pelage follicles

absent Meibomian glands ( J:71744 )

abnormal sweat gland morphology ( J:71744 )

• the sweat glands are absent in the foot pads

abnormal coat/ hair morphology ( J:71744 )

• the only hair type found in mutants reaching adulthood is a monotrich-awl intermediate

abnormal coat appearance ( J:71744 )

• mutants reaching adulthood have shaggy fur

abnormal hair growth ( J:71744 )

• mutants reaching adulthood have no hair on the tail and behind the ears

alopecia ( J:71744 )

• patchy alopecia in older mice

abnormal hair follicle development ( J:71744 )

• hair follicles develop at a slower rate

absent hair follicles ( J:71744 )

• no anlagen for hair follicles is seen in the tail

decreased hair follicle number ( J:71744 )

• newborns produce very few hair follicles and the reduced number of hair follicles persists throughout adulthood

abnormal vibrissa follicle morphology ( J:71744 )

• mutants exhibit an increased rate of apoptosis in many vibrissal follicles

sparse vibrissae ( J:71744 )

• mutants reaching adulthood have fewer vibrissae

cellular

abnormal intestinal goblet cell morphology ( J:71744 )

• reduction in the number of intestinal goblet cells

increased hair follicle apoptosis ( J:71744 )

• mutants exhibit an increased rate of apoptosis in many pelage follicles

increased hepatocyte apoptosis ( J:71744 )

• livers show an increase in embryonic (E12.5-14.5) hepatocyte apoptosis

• however, mutants surviving to birth and adulthood, do not show gross liver abnormalities

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
otitis media		DOID:10754		J:71744

Genotype
MGI:5430609

ht3

• Allelic Composition: Ctnnb1^tm1.2Wvv/Ctnnb1⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

neoplasm

increased gastrointestinal tumor incidence ( J:185942 )

• 14 tumors at 16-18 months in the duodenum and jejunum in 11 of 29 mice examined compared to none in controls

• 50% gastrointestinal intraepithelial neoplasia/adenoma

increased intestinal adenocarcinoma incidence ( J:185942 )

• 29% are dysplastic adenoma/carcinoma

increased intestinal adenoma incidence ( J:185942 )

• 21% of total

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:185942 )

• 14 tumors at 16-18 months in the duodenum and jejunum in 11 of 29 mice examined compared to none in controls

• 50% gastrointestinal intraepithelial neoplasia/adenoma

increased intestinal adenocarcinoma incidence ( J:185942 )

• 29% are dysplastic adenoma/carcinoma

increased intestinal adenoma incidence ( J:185942 )

• 21% of total

Genotype
MGI:4943530

ht4

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺
• Genetic Background: involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ

neoplasm

increased intestinal adenoma incidence ( J:169830 )

• adults receiving a single tamoxifen dose at P60 demonstrated numerous microadenomas in the small intestines when analyzed at P105

digestive/alimentary system

abnormal small intestinal crypt cell proliferation ( J:169830 )

• adults receiving a single tamoxifen dose at P60 and analyzed at P105 show an expansion of the proliferative compartment from crypts to more distal epithelium

abnormal small intestine morphology ( J:169830 )

• adults receiving a single tamoxifen dose at P60 and analyzed at P105 show a general tissue disorganization of the small intestine

increased intestinal adenoma incidence ( J:169830 )

• adults receiving a single tamoxifen dose at P60 demonstrated numerous microadenomas in the small intestines when analyzed at P105

cellular

abnormal small intestinal crypt cell proliferation ( J:169830 )

• adults receiving a single tamoxifen dose at P60 and analyzed at P105 show an expansion of the proliferative compartment from crypts to more distal epithelium

Genotype
MGI:2673885

ht5

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺
• Genetic Background: involves: 129X1/SvJ

normal phenotype

no abnormal phenotype detected ( J:58367 )

Genotype
MGI:2656754

ht6

• Allelic Composition: Ctnnb1^Bfc/Ctnnb1⁺
• Genetic Background: involves: BALB/cCrl * C3H/HeNCrl

craniofacial

broad head ( J:63816 , J:209611 )

• broad face (J:63816)

• the anteroposterior axis was significantly shortened, whereas the dorsoventral and medial-lateral axes were enlarged (J:209611)

vision/eye

ocular hypertelorism ( J:63816 )

• wide-spaced eyes

growth/size/body

broad head ( J:63816 , J:209611 )

• broad face (J:63816)

• the anteroposterior axis was significantly shortened, whereas the dorsoventral and medial-lateral axes were enlarged (J:209611)

nervous system

increased brain size ( J:209611 )

• gray matter and total brain volumes were significantly larger in Bfc/+ (P < 0.05; 1-way ANOVA)

decreased corpus callosum size ( J:209611 )

• the corpus callosum appeared to be severely underdeveloped in 3 Bfc/+ individuals, and lacked any inter-hemispheric extensions

abnormal globus pallidus morphology ( J:209611 )

• globus pallidus is slightly, but significantly, larger in Bfc/+

increased striatum size ( J:209611 )

• striatum is slightly, but significantly, larger in Bfc/+

enlarged thalamus ( J:209611 )

• thalamus is slightly, but significantly, larger in Bfc/+

abnormal hippocampus neuron morphology ( J:209611 )

• the length and number of neurites were significantly increased after only 1 day in culture

• after 8 days in culture, the extent of dendritic branching in heterozygous neurons was dramatically lower than in controls

small olfactory bulb ( J:209611 )

• mutants showed substantially reduced cerebellar and olfactory bulb volumes compared with controls

small cerebellum ( J:209611 )

• mutants showed substantially reduced cerebellar and olfactory bulb volumes compared with controls

abnormal synaptic vesicle clustering ( J:209611 )

• heterozygotes, a lower density of docked synaptic vesicles (SV) in cortex and in hippocampus CA1 region is seen

reduced long-term potentiation ( J:209611 )

• long-term potentiation (LTP) induced by either tetanic or theta-burst stimulation was significantly reduced in hippocampus CA1 slices from heterozygous mice

decreased prepulse inhibition ( J:209611 )

• heterozygous mice mice show significant PPI deficits but acoustic startle response is comparable to controls

behavior/neurological

impaired contextual conditioning behavior ( J:209611 )

• freezing behavior in heterozygous mice using a standard fear conditioning protocol for contextual memory is significantly lower than that of littermate controls, suggesting that mutants have a reduced capacity to recall the previous shock exposure

abnormal operant conditioning behavior ( J:209611 )

• for trials in which rewards are given after a light event, responses increase significantly during the expected time interval in control mice, but not in heterozygous mutants

• in probe trials where no reward is given, responses of heterozygous mutant mice during the critical time window is significantly lower than littermate controls

abnormal spatial reference memory ( J:209611 )

• control animals improve performance with repeated trials in the hidden platform variation of the water maze test, but heterozygous mutant mice did not improve

impaired coordination ( J:209611 )

• heterozygous mice show a significantly shorter latency period before falling from the rod in a challenging rotarod test incorporaing 6 consecutive accelerating stages in a single session; no differences are seen in a standard rotarod test

abnormal vocalization ( J:209611 )

• heterozygous pups exhibit a significant reduction in the total number of vocalizations with more of these calls characterized by a single component compared to controls

Genotype
MGI:3706583

cn7

• Allelic Composition: Ctnnb1^{tm2(Nfkbia)Rsu}/Ctnnb1⁺; Tg(Myh6-cre)2182Mds/0
• Genetic Background: B6.Cg-Ctnnb1^{tm2(Nfkbia)Rsu} Tg(Myh6-cre)2182Mds

cardiovascular system

decreased response of heart to induced stress ( J:111645 )

• mutants display an attenuated hypertrophic response compared with controls upon infusion of angiotensin II or isoproterenol as well as reduced expression of hypertrophy markers

homeostasis/metabolism

decreased response of heart to induced stress ( J:111645 )

• mutants display an attenuated hypertrophic response compared with controls upon infusion of angiotensin II or isoproterenol as well as reduced expression of hypertrophy markers

Genotype
MGI:5576521

cn8

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Wap-cre)11738Mam/0
• Genetic Background: FVB.Cg-Ctnnb1^tm1Mmt Tg(Wap-cre)11738Mam

neoplasm

increased mammary gland tumor incidence in breeding females ( J:206839 )

♀ • the majority of females develop mammary gland tumors between 25 and 40 weeks postpartum

♀ • tumors are squamous metaplasia

endocrine/exocrine glands

increased mammary gland tumor incidence in breeding females ( J:206839 )

♀ • the majority of females develop mammary gland tumors between 25 and 40 weeks postpartum

♀ • tumors are squamous metaplasia

integument

increased mammary gland tumor incidence in breeding females ( J:206839 )

♀ • the majority of females develop mammary gland tumors between 25 and 40 weeks postpartum

♀ • tumors are squamous metaplasia

Genotype
MGI:5576520

cn9

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Wap-cre)11738Mam/0; Tg(Wap-Hgf)402Mig/0
• Genetic Background: FVB.Cg-Ctnnb1^tm1Mmt Tg(Wap-cre)11738Mam Tg(Wap-Hgf)402Mig

neoplasm

increased mammary gland tumor incidence in breeding females ( J:206839 )

♀ • tumor onset is more rapid than in either single mutant, with almost all females showing mammary gland tumors by 2 weeks postpartum

♀ • tumors exhibit a mixed phenotype, with areas resembling basaloid hyperplasia and squamous metaplasia

♀ • tumors exhibit morphological, gene and protein expression profile characteristics of basal breast cancers; they are HER2/ErbB2, ER, and PR negative, and express metastasis-associated genes

♀ • treatment with the Wnt and Met inhibitors ICG-001 or PHA 665752 results in a moderate decrease in mammary gland tumor volume, treatment with a combination of these or with a small molecule inhibitor AMD3100, an agonist of CXCR4 receptor, strongly suppresses tumor onset up to 16 days, and treatment with all three shows the strongest inhibition in tumor size

increased mammary gland tumor incidence in virgin females ( J:206839 )

♀ • in a few cases, virgin females develop small tumors

endocrine/exocrine glands

abnormal mammary gland morphology ( J:206839 )

♀ • mammary gland tissues of breeding females show an expansion of CD24+/CD29(medium) and CD24+/CD49(hi) cells and depletion of CD24(low)/CD29+ cells, indicating expansion of a population of cells with progenitor and stem cell characteristics

abnormal mammary gland growth during lactation ( J:206839 )

♀ • production of milk protein beta-casein after pregnancy is not detected indicating a block in normal mammary gland differentiation

mammary gland alveolar hyperplasia ( J:206839 )

♀ • lobuloalveolar hyperplasia

increased mammary gland tumor incidence in breeding females ( J:206839 )

♀ • tumor onset is more rapid than in either single mutant, with almost all females showing mammary gland tumors by 2 weeks postpartum

♀ • tumors exhibit a mixed phenotype, with areas resembling basaloid hyperplasia and squamous metaplasia

♀ • tumors exhibit morphological, gene and protein expression profile characteristics of basal breast cancers; they are HER2/ErbB2, ER, and PR negative, and express metastasis-associated genes

♀ • treatment with the Wnt and Met inhibitors ICG-001 or PHA 665752 results in a moderate decrease in mammary gland tumor volume, treatment with a combination of these or with a small molecule inhibitor AMD3100, an agonist of CXCR4 receptor, strongly suppresses tumor onset up to 16 days, and treatment with all three shows the strongest inhibition in tumor size

increased mammary gland tumor incidence in virgin females ( J:206839 )

♀ • in a few cases, virgin females develop small tumors

integument

abnormal mammary gland morphology ( J:206839 )

♀ • mammary gland tissues of breeding females show an expansion of CD24+/CD29(medium) and CD24+/CD49(hi) cells and depletion of CD24(low)/CD29+ cells, indicating expansion of a population of cells with progenitor and stem cell characteristics

abnormal mammary gland growth during lactation ( J:206839 )

♀ • production of milk protein beta-casein after pregnancy is not detected indicating a block in normal mammary gland differentiation

mammary gland alveolar hyperplasia ( J:206839 )

♀ • lobuloalveolar hyperplasia

increased mammary gland tumor incidence in breeding females ( J:206839 )

♀ • tumor onset is more rapid than in either single mutant, with almost all females showing mammary gland tumors by 2 weeks postpartum

♀ • tumors exhibit a mixed phenotype, with areas resembling basaloid hyperplasia and squamous metaplasia

♀ • tumors exhibit morphological, gene and protein expression profile characteristics of basal breast cancers; they are HER2/ErbB2, ER, and PR negative, and express metastasis-associated genes

♀ • treatment with the Wnt and Met inhibitors ICG-001 or PHA 665752 results in a moderate decrease in mammary gland tumor volume, treatment with a combination of these or with a small molecule inhibitor AMD3100, an agonist of CXCR4 receptor, strongly suppresses tumor onset up to 16 days, and treatment with all three shows the strongest inhibition in tumor size

increased mammary gland tumor incidence in virgin females ( J:206839 )

♀ • in a few cases, virgin females develop small tumors

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
breast cancer		DOID:1612	OMIM:114480	J:206839

Genotype
MGI:5576532

cn10

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Cxcr4^tm2Yzo/Cxcr4^tm2Yzo; Tg(Wap-cre)11738Mam/0; Tg(Wap-Hgf)402Mig/0
• Genetic Background: FVB.Cg-Cxcr4^tm2Yzo Ctnnb1^tm1Mmt Tg(Wap-cre)11738Mam Tg(Wap-Hgf)402Mig

neoplasm

decreased mammary gland tumor incidence in breeding females ( J:206839 )

♀ • appearance of mammary tumors in postpartum females is delayed compared to triple Ctnnb1^tm1Mmt Tg(Wap-cre)11738Mam Tg(Wap-Hgf)402Mig mutants, with tumors developing at 7 weeks postpartum rather than 2 weeks

♀ • tumors are smaller in females 2 weeks postpartum than in triple mutants

endocrine/exocrine glands

decreased mammary gland tumor incidence in breeding females ( J:206839 )

♀ • appearance of mammary tumors in postpartum females is delayed compared to triple Ctnnb1^tm1Mmt Tg(Wap-cre)11738Mam Tg(Wap-Hgf)402Mig mutants, with tumors developing at 7 weeks postpartum rather than 2 weeks

♀ • tumors are smaller in females 2 weeks postpartum than in triple mutants

integument

decreased mammary gland tumor incidence in breeding females ( J:206839 )

♀ • appearance of mammary tumors in postpartum females is delayed compared to triple Ctnnb1^tm1Mmt Tg(Wap-cre)11738Mam Tg(Wap-Hgf)402Mig mutants, with tumors developing at 7 weeks postpartum rather than 2 weeks

♀ • tumors are smaller in females 2 weeks postpartum than in triple mutants

Genotype
MGI:5546509

cn11

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Msx2-rtTA)885Lma/0; Tg(tetO-cre)1Jaw/0
• Genetic Background: involves: 129 * 129X1/SvJ * C57BL/6

craniofacial

abnormal craniofacial morphology ( J:202618 )

• mutants on a doxycycline diet exhibit craniofacial malformations

integument

alopecia ( J:202618 )

• mutants on a doxycycline diet exhibit alopecia

mortality/aging

premature death ( J:202618 )

• 35% of mutants on a doxycycline diet for at least 3 weeks starting at P25 die during the 12 weeks following doxycycline administration; males and females die at similar rates

renal/urinary system

abnormal urinary bladder morphology ( J:202618 )

• urothelia of males on the doxycycline diet is more severely affected than in females

• increase in urothelial basal cell proliferation is seen in mutants fed doxycycline

• bladders of males 5 weeks after doxycline treatment show a higher proliferation index than females at the same stage

increased urinary bladder carcinoma incidence ( J:202618 )

• 24% of the remaining surviving mutants on a doxycycline diet for at least 3 weeks starting at P25 exhibit tumors within the bladder lumen; 11 mutants have single tumor and 18 have multifoci tumors

• tumors in doxycline fed mutants resemble low-grade papillary urothelial carcinoma, exhibit polypoid structure, and the urothelium has lost its typical polarity and shows nuclear atypia, high mitogenic activity, and vascular infiltration

• however, no nuclear pleomorphism or muscle invasion is seen

• 45% of males on the doxycycline diet develop bladder tumors compared to 3% of females on the diet

• only 12.5% of castrated males after 3 months of doxycycline treatment develop luminal tumors and cell proliferation is 20% less than in noncastrated males

neoplasm

increased urinary bladder carcinoma incidence ( J:202618 )

• 24% of the remaining surviving mutants on a doxycycline diet for at least 3 weeks starting at P25 exhibit tumors within the bladder lumen; 11 mutants have single tumor and 18 have multifoci tumors

• tumors in doxycline fed mutants resemble low-grade papillary urothelial carcinoma, exhibit polypoid structure, and the urothelium has lost its typical polarity and shows nuclear atypia, high mitogenic activity, and vascular infiltration

• however, no nuclear pleomorphism or muscle invasion is seen

• 45% of males on the doxycycline diet develop bladder tumors compared to 3% of females on the diet

• only 12.5% of castrated males after 3 months of doxycycline treatment develop luminal tumors and cell proliferation is 20% less than in noncastrated males

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
urinary bladder cancer		DOID:11054	OMIM:109800	J:202618

Genotype
MGI:4429127

cn12

• Allelic Composition: Ctnnb1^tm2Kem/Ctnnb1⁺; Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy}/Gt(ROSA)26Sor⁺; Tg(Col2a1-cre)1Bhr/0; Tg(tetO-Vegfa)90Ala/0
• Genetic Background: involves: 129 * C57BL/6 * FVB/N * ICR * SJL

neoplasm

increased hemangioma incidence ( J:156474 )

• local bone and marrow tissue in doxycycline-treat mice are replaced with massively enlarged vascular structures (hemangiomas) unlike in wild-type mice

skeleton

skeleton phenotype ( J:156474 )

N • doxycycline-treat mice exhibit normal bone density, osteoclastic bone remodeling, and bone degradation

Genotype
MGI:5086016

cn13

• Allelic Composition: Ctnnb1^tm2Kem/Ctnnb1⁺; Tg(Prrx1-cre)1Cjt/0
• Genetic Background: involves: 129 * C57BL/6 * SJL

skeleton

abnormal skeleton morphology ( J:173242 )

• slight reduction in bone size

Genotype
MGI:5086015

cn14

• Allelic Composition: Ctnnb1^tm2Kem/Ctnnb1⁺; Amer1^tm1.1Nbar/Y; Tg(Prrx1-cre)1Cjt/0
• Genetic Background: involves: 129 * C57BL/6 * SJL

skeleton

skeleton phenotype ( J:173242 )

♂N • suppression of bone abnormalities (malformation of the deltoid tuberosity and sternum and accumulation of cortical bone) seen in mutant mice wild-type for Ctnnb1

Genotype
MGI:5435570

cn15

• Allelic Composition: Ctnnb1^tm4Wbm/Ctnnb1⁺; Tg(KRT14-cre)1Efu/0
• Genetic Background: involves: 129P2/OlaHsd

Lack of hair follicles in Ctnnb1^tm4Wbm/Ctnnb1⁺ Tg(KRT14-cre)1Efu/0 mice

integument

alopecia ( J:186934 )

absent hair follicles ( J:186934 )

Genotype
MGI:5314537

cn16

• Allelic Composition: Ctnnb1^tm2Kem/Ctnnb1⁺; Hesx1^tm1(cre)Jpmb/Hesx1^tm1Icar
• Genetic Background: involves: 129P2/OlaHsd * 129S * 129X1/SvJ * C57BL/6

nervous system

abnormal forebrain development ( J:181005 )

small embryonic telencephalon ( J:181005 )

• in some mice

vision/eye

microphthalmia ( J:181005 )

• bilateral in some mice

• unilateral in some mice

anophthalmia ( J:181005 )

• unilateral in some mice

Genotype
MGI:5581947

cn17

• Allelic Composition: Ctnnb1^tm2Kem/Ctnnb1⁺; Lyz2^tm1(cre)Ifo/Lyz2⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

skeleton

increased osteoclast cell number ( J:178340 )

decreased trabecular bone volume ( J:178340 )

osteoporosis ( J:178340 )

increased bone resorption ( J:178340 )

hematopoietic system

increased osteoclast cell number ( J:178340 )

immune system

increased osteoclast cell number ( J:178340 )

Genotype
MGI:5581952

cn18

• Allelic Composition: Ctnnb1^tm2Kem/Ctnnb1⁺; Pparg^{tm1.1(tTA)Jmgr}/Pparg⁺; Tg(tetO-cre)1Jaw/0
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6

skeleton

skeleton phenotype ( J:178340 )

N • doxycycline-treated mice exhibit normal numbers of osteoblasts, bone formation and bone mineral apposition rates

increased osteoclast cell number ( J:178340 )

• in doxycycline-treated mice

abnormal osteoclast physiology ( J:178340 )

• doxycycline-treated bone marrow cultures exhibit reduced osteoclast precursor proliferation compared with control cultures

abnormal trabecular bone morphology ( J:178340 )

• decreased bone surface in doxycycline-treated mice

decreased trabecular bone volume ( J:178340 )

• trabecular, cortical and total in doxycycline-treated mice

decreased bone trabecula number ( J:178340 )

• with increased spacing in doxycycline-treated mice

decreased trabecular bone mass ( J:178340 )

• in doxycycline-treated mice

decreased trabecular bone thickness ( J:178340 )

• in doxycycline-treated mice

osteoporosis ( J:178340 )

• in doxycycline-treated mice

increased bone resorption ( J:178340 )

• in doxycycline-treated mice

hematopoietic system

increased osteoclast cell number ( J:178340 )

• in doxycycline-treated mice

abnormal osteoclast physiology ( J:178340 )

• doxycycline-treated bone marrow cultures exhibit reduced osteoclast precursor proliferation compared with control cultures

immune system

increased osteoclast cell number ( J:178340 )

• in doxycycline-treated mice

abnormal osteoclast physiology ( J:178340 )

• doxycycline-treated bone marrow cultures exhibit reduced osteoclast precursor proliferation compared with control cultures

Genotype
MGI:5508218

cn19

• Allelic Composition: Bmpr1a^tm2.1Bhr/Bmpr1a^tm2.1Bhr; Ctnnb1^tm1Mmt/Ctnnb1⁺; Krt14^{tm1.1(cre)Wbm}/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * 129X1/SvJ

mortality/aging

decreased tumor-free survival time ( J:199091 )

• mutants succumb to tumors rapidly, dying between P75 and P90

neoplasm

increased salivary gland tumor incidence ( J:199091 )

• rapidly develop aggressive tumors in the salivary glands

• tumors contain transplantable and hyperproliferative tumor propagating cells (CD24+CD29+)

• treatment of cultured CD24+CD29+ tumor cells with the canonical Wnt inhibitor ICG-001 blocks proliferation of these cells

• CD24+CD29+ tumor propagating cells from salivary gland tumors exhibit unrestricted self-renewal in salisphere culture

increased squamous cell carcinoma incidence ( J:199091 )

• tumors arise from the submandibular salivary glands and are classified as salivary gland squamous cell carcinoma

digestive/alimentary system

increased salivary gland tumor incidence ( J:199091 )

• rapidly develop aggressive tumors in the salivary glands

• tumors contain transplantable and hyperproliferative tumor propagating cells (CD24+CD29+)

• treatment of cultured CD24+CD29+ tumor cells with the canonical Wnt inhibitor ICG-001 blocks proliferation of these cells

• CD24+CD29+ tumor propagating cells from salivary gland tumors exhibit unrestricted self-renewal in salisphere culture

endocrine/exocrine glands

increased salivary gland tumor incidence ( J:199091 )

• rapidly develop aggressive tumors in the salivary glands

• tumors contain transplantable and hyperproliferative tumor propagating cells (CD24+CD29+)

• treatment of cultured CD24+CD29+ tumor cells with the canonical Wnt inhibitor ICG-001 blocks proliferation of these cells

• CD24+CD29+ tumor propagating cells from salivary gland tumors exhibit unrestricted self-renewal in salisphere culture

integument

increased hair follicle number ( J:199091 )

• excessive supernumerary hair follicles in the skin

craniofacial

increased salivary gland tumor incidence ( J:199091 )

• rapidly develop aggressive tumors in the salivary glands

• tumors contain transplantable and hyperproliferative tumor propagating cells (CD24+CD29+)

• treatment of cultured CD24+CD29+ tumor cells with the canonical Wnt inhibitor ICG-001 blocks proliferation of these cells

• CD24+CD29+ tumor propagating cells from salivary gland tumors exhibit unrestricted self-renewal in salisphere culture

growth/size/body

increased salivary gland tumor incidence ( J:199091 )

• rapidly develop aggressive tumors in the salivary glands

• tumors contain transplantable and hyperproliferative tumor propagating cells (CD24+CD29+)

• treatment of cultured CD24+CD29+ tumor cells with the canonical Wnt inhibitor ICG-001 blocks proliferation of these cells

• CD24+CD29+ tumor propagating cells from salivary gland tumors exhibit unrestricted self-renewal in salisphere culture

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
salivary gland carcinoma		DOID:0050904		J:199091

Genotype
MGI:5508224

cn20

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Krt14^{tm1.1(cre)Wbm}/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ

neoplasm

neoplasm ( J:199091 )

N • mice do not develop salivary squamous cell carcinoma

Genotype
MGI:5475209

cn21

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Lgr5^{tm1(cre/ERT2)Cle}/Lgr5⁺
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ

digestive/alimentary system

intestine polyps ( J:193873 )

• 40 days after tamoxifen treatment, mice have developed numerous polyps

Genotype
MGI:5581954

cn22

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Lyz2^tm1(cre)Ifo/Lyz2⁺
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ

skeleton

skeleton phenotype ( J:178340 )

N • mice exhibit normal bone formation

abnormal osteoclast differentiation ( J:178340 )

• impaired

increased bone volume ( J:178340 )

decreased bone resorption ( J:178340 )

hematopoietic system

abnormal osteoclast differentiation ( J:178340 )

• impaired

decreased bone marrow cell number ( J:178340 )

cellular

abnormal osteoclast differentiation ( J:178340 )

• impaired

immune system

abnormal osteoclast differentiation ( J:178340 )

• impaired

Genotype
MGI:5581956

cn23

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Pparg^{tm1.1(tTA)Jmgr}/Pparg⁺; Tg(tetO-cre)1Jaw/0
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6

skeleton

skeleton phenotype ( J:178340 )

N • doxycycline-treated mice exhibit normal bone formation and numbers of osteoblasts

abnormal osteoclast differentiation ( J:178340 )

• impaired in doxycycline-treated mice

decreased osteoclast cell number ( J:178340 )

• in doxycycline-treated mice

increased bone volume ( J:178340 )

• as early as P15 in doxycycline-treated mice

• 27-fold from 10 months of age in doxycycline-treated mice

increased compact bone volume ( J:178340 )

• in doxycycline-treated mice

abnormal trabecular bone morphology ( J:178340 )

• 4.6-fold increase in trabecular bone surface and a smaller bone surface to bone volume in doxycycline-treated mice

increased trabecular bone volume ( J:178340 )

• trabecular, cortical and total volume as early as P15 in doxycycline-treated mice

increased bone trabecula number ( J:178340 )

• 3.6-fold with reduced trabecular separation in doxycycline-treated mice

increased trabecular bone thickness ( J:178340 )

• 8.5-fold in doxycycline-treated mice

osteopetrosis ( J:178340 )

• severe in doxycycline-treated mice

• in mice following adult onset activation with doxycycline

decreased bone resorption ( J:178340 )

• in doxycycline-treated mice

hematopoietic system

abnormal osteoclast differentiation ( J:178340 )

• impaired in doxycycline-treated mice

extramedullary hematopoiesis ( J:178340 )

• in doxycycline-treated mice

decreased bone marrow cell number ( J:178340 )

• at 4 months in doxycycline-treated mice

absent bone marrow cell ( J:178340 )

• at 10 months in doxycycline-treated mice

decreased osteoclast cell number ( J:178340 )

• in doxycycline-treated mice

increased splenocyte number ( J:178340 )

• gradual in doxycycline-treated mice

cellular

abnormal osteoclast differentiation ( J:178340 )

• impaired in doxycycline-treated mice

immune system

abnormal osteoclast differentiation ( J:178340 )

• impaired in doxycycline-treated mice

decreased osteoclast cell number ( J:178340 )

• in doxycycline-treated mice

increased splenocyte number ( J:178340 )

• gradual in doxycycline-treated mice

Genotype
MGI:5512969

cn24

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Sox2^{tm1.1(cre/ERT2)Jpmb}/Sox2⁺
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6

neoplasm

increased pituitary gland tumor incidence ( J:201265 )

• with 2 low doses of tamoxifen given at 6 weeks, most mice display obvious pituitary tumors between 3 and 5 months upon necropsy; pituitaries of remaining animals contained small tumors in the anterior lobe upon histological analysis

endocrine/exocrine glands

abnormal adenohypophysis morphology ( J:201265 )

• at E15.5, embryos show an enlarged anterior pituitary, with foci of accumulation of beta-catenin when tamoxifen induction is done at E10.5; clusters are observed to contain undifferentiated cells that do not express proliferation marker Ki67

increased pituitary gland tumor incidence ( J:201265 )

• with 2 low doses of tamoxifen given at 6 weeks, most mice display obvious pituitary tumors between 3 and 5 months upon necropsy; pituitaries of remaining animals contained small tumors in the anterior lobe upon histological analysis

nervous system

abnormal adenohypophysis morphology ( J:201265 )

• at E15.5, embryos show an enlarged anterior pituitary, with foci of accumulation of beta-catenin when tamoxifen induction is done at E10.5; clusters are observed to contain undifferentiated cells that do not express proliferation marker Ki67

increased pituitary gland tumor incidence ( J:201265 )

• with 2 low doses of tamoxifen given at 6 weeks, most mice display obvious pituitary tumors between 3 and 5 months upon necropsy; pituitaries of remaining animals contained small tumors in the anterior lobe upon histological analysis

Genotype
MGI:5438217

cn25

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Pik3ca^tm1Gilb/Pik3ca⁺; Trp53^tm1Brn/Trp53⁺; Tg(Fabp7-cre,-lacZ)3Gtm/0
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * CBA

neoplasm

increased medulloblastoma incidence ( J:186709 )

• by 3 months of age, all mice develop WNT-subgroup medulloblastomas

nervous system

increased medulloblastoma incidence ( J:186709 )

• by 3 months of age, all mice develop WNT-subgroup medulloblastomas

Genotype
MGI:5438218

cn26

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Trp53^tm1Brn/Trp53⁺; Tg(Fabp7-cre,-lacZ)3Gtm/0
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * CBA

neoplasm

increased medulloblastoma incidence ( J:186709 )

• by 11 months, 4% of mice develop WNT-subgroup medulloblastomas

nervous system

increased medulloblastoma incidence ( J:186709 )

• by 11 months, 4% of mice develop WNT-subgroup medulloblastomas

Genotype
MGI:3706580

cn27

• Allelic Composition: Ctnnb1^{tm2(Nfkbia)Rsu}/Ctnnb1⁺; Tg(CMV-cre)1Cgn/0
• Genetic Background: involves: 129P2/OlaHsd * BALB/cJ * C57BL/6

mortality/aging

prenatal lethality, incomplete penetrance ( J:71744 )

• authors state the they observe all phenotypic features of heterozygous Ctnnb1^{tm1(Nfkbia)Rsu} mutants in these mice, however no data is presented in J:71744

immune system

increased leukocyte cell number ( J:71744 )

increased granulocyte number ( J:71744 )

abnormal macrophage physiology ( J:71744 )

abnormal Peyer's patch morphology ( J:71744 )

abnormal lymph node morphology ( J:71744 )

increased inflammatory response ( J:71744 )

increased susceptibility to otitis media ( J:71744 )

keratoconjunctivitis sicca ( J:71744 )

vision/eye

keratoconjunctivitis sicca ( J:71744 )

abnormal eye morphology ( J:71744 )

abnormal eyelid morphology ( J:71744 )

absent Meibomian glands ( J:71744 )

blindness ( J:71744 )

dry eyes ( J:71744 )

growth/size/body

abnormal incisor morphology ( J:71744 )

abnormal molar morphology ( J:71744 )

decreased body size ( J:71744 )

• about 50-70% of wild-type

endocrine/exocrine glands

absent Meibomian glands ( J:71744 )

Harderian gland atrophy ( J:71744 )

• atrophy of Harderian glands

hearing/vestibular/ear

deafness ( J:71744 )

increased susceptibility to otitis media ( J:71744 )

digestive/alimentary system

gastrointestinal hemorrhage ( J:71744 )

abnormal intestinal goblet cell morphology ( J:71744 )

• reduction in the number of intestinal goblet cells

abnormal small intestine morphology ( J:71744 )

• the epithelial structure of the small intestine is loosened

cardiovascular system

gastrointestinal hemorrhage ( J:71744 )

liver hemorrhage ( J:71744 )

craniofacial

abnormal incisor morphology ( J:71744 )

abnormal molar morphology ( J:71744 )

domed cranium ( J:71744 )

hematopoietic system

increased leukocyte cell number ( J:71744 )

increased granulocyte number ( J:71744 )

abnormal macrophage physiology ( J:71744 )

liver/biliary system

liver hemorrhage ( J:71744 )

increased hepatocyte apoptosis ( J:71744 )

• in embryos only

reproductive system

decreased litter size ( J:71744 )

skeleton

abnormal incisor morphology ( J:71744 )

abnormal molar morphology ( J:71744 )

domed cranium ( J:71744 )

limbs/digits/tail

kinked tail ( J:71744 )

behavior/neurological

lethargy ( J:71744 )

tremors ( J:71744 )

hunched posture ( J:71744 )

integument

absent Meibomian glands ( J:71744 )

abnormal hair growth ( J:71744 )

alopecia ( J:71744 )

• patchy alopecia in older mice

sparse hair ( J:71744 )

• thin fur

abnormal hair follicle development ( J:71744 )

sparse vibrissae ( J:71744 )

cellular

abnormal intestinal goblet cell morphology ( J:71744 )

• reduction in the number of intestinal goblet cells

increased hepatocyte apoptosis ( J:71744 )

• in embryos only

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
otitis media		DOID:10754		J:71744

Genotype
MGI:5430612

cn28

• Allelic Composition: Apc^tm1Rsmi/Apc⁺; Ctnnb1^tm1Wvv/Ctnnb1⁺; Tg(Fabp1-cre)1Jig/?
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J * FVB/N

neoplasm

increased gastrointestinal tumor incidence ( J:185942 )

• significantly increased tumor load in the intestine of males but not females compared to heterozygous Apc^tm1Ecrm

• tumors in both the ilium and colon but smaller in size than in heterozygous Apc^tm1Ecrm

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:185942 )

• significantly increased tumor load in the intestine of males but not females compared to heterozygous Apc^tm1Ecrm

• tumors in both the ilium and colon but smaller in size than in heterozygous Apc^tm1Ecrm

Genotype
MGI:4839562

cn29

• Allelic Composition: Ctnnb1^tm2Kem/Ctnnb1⁺; Pten^tm1Hwu/Pten^tm1Hwu; Tg(Cdh5-cre)7Mlia/0
• Genetic Background: involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * BALB/c * C57BL/6 * FVB/N

mortality/aging

premature death ( J:135172 )

• die before P68 with vascular complications

hematopoietic system

abnormal definitive hematopoiesis ( J:135172 )

• 100% of mutants develop myeloproliferative disorder at about P30

cardiovascular system

abnormal blood vessel morphology ( J:135172 )

• mutants exhibit vascular complication

Genotype
MGI:3805821

cn30

• Allelic Composition: Bmi1^{tm1(cre/ERT)Mrc}/Bmi1⁺; Ctnnb1^tm1Mmt/Ctnnb1⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

mortality/aging

premature death ( J:138364 )

• mice die 50 days following administration of tamoxifen

neoplasm

increased intestinal adenoma incidence ( J:138364 )

• beginning 22 days following administration of tamoxifen

digestive/alimentary system

abnormal crypts of Lieberkuhn morphology ( J:138364 )

• the number of proliferating cells within crypts is increased 15 days following administration of tamoxifen

increased intestinal adenoma incidence ( J:138364 )

• beginning 22 days following administration of tamoxifen

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:138364 )

• the number of proliferating cells within crypts is increased 15 days following administration of tamoxifen

Genotype
MGI:4365782

cn31

• Allelic Composition: Ctnnb1^tm2Kem/Ctnnb1⁺; Osr2^tm2(cre)Jian/Osr2⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

skeleton

abnormal enamel knot morphology ( J:153554 )

• unlike in wild-type mice, strong Caspase3 activity is detected in the enamel knot cells of the maxillary and mandibular first molar tooth germs at E14.5

• however, no increase in cell death in tooth epithelium and mesenchyme is detected

growth retardation of incisors ( J:153554 )

• incisor development arrests at bud stage

growth retardation of molars ( J:153554 )

• molar development arrests at bud stage

mortality/aging

neonatal lethality ( J:153554 )

craniofacial

abnormal enamel knot morphology ( J:153554 )

• unlike in wild-type mice, strong Caspase3 activity is detected in the enamel knot cells of the maxillary and mandibular first molar tooth germs at E14.5

• however, no increase in cell death in tooth epithelium and mesenchyme is detected

growth retardation of incisors ( J:153554 )

• incisor development arrests at bud stage

growth retardation of molars ( J:153554 )

• molar development arrests at bud stage

cleft secondary palate ( J:153554 )

digestive/alimentary system

cleft secondary palate ( J:153554 )

growth/size/body

abnormal enamel knot morphology ( J:153554 )

• unlike in wild-type mice, strong Caspase3 activity is detected in the enamel knot cells of the maxillary and mandibular first molar tooth germs at E14.5

• however, no increase in cell death in tooth epithelium and mesenchyme is detected

growth retardation of incisors ( J:153554 )

• incisor development arrests at bud stage

growth retardation of molars ( J:153554 )

• molar development arrests at bud stage

cleft secondary palate ( J:153554 )

Genotype
MGI:3836578

cn32

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Kras^tm1Bbd/Kras⁺; Tg(Pbsn-cre)4Prb/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2

mortality/aging

premature death ( J:143034 )

• mice die prior to day 300

reproductive system

squamous metaplasia of bulbourethral gland ( J:143034 )

♂ • mice exhibit keratinized squamous metaplasia in the bulbourethral gland unlike wild-type mice

increased prostate gland tumor incidence ( J:143034 )

♂ • all mice develop diffuse, locally invasive carcinomas in the prostate that develop from solid or sheet-like proliferation with occasional rosette structures, nuclear atypia, apoptotic bodies, and mitosis unlike in wild-type mice

neoplasm

increased prostate gland tumor incidence ( J:143034 )

♂ • all mice develop diffuse, locally invasive carcinomas in the prostate that develop from solid or sheet-like proliferation with occasional rosette structures, nuclear atypia, apoptotic bodies, and mitosis unlike in wild-type mice

renal/urinary system

squamous metaplasia of urethral gland ( J:143034 )

• mice exhibit keratinized squamous metaplasia in the urethral gland unlike wild-type mice

endocrine/exocrine glands

squamous metaplasia of bulbourethral gland ( J:143034 )

♂ • mice exhibit keratinized squamous metaplasia in the bulbourethral gland unlike wild-type mice

increased prostate gland tumor incidence ( J:143034 )

♂ • all mice develop diffuse, locally invasive carcinomas in the prostate that develop from solid or sheet-like proliferation with occasional rosette structures, nuclear atypia, apoptotic bodies, and mitosis unlike in wild-type mice

squamous metaplasia of urethral gland ( J:143034 )

• mice exhibit keratinized squamous metaplasia in the urethral gland unlike wild-type mice

Genotype
MGI:6507888

cn33

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Igs2^{tm1(CAG-Met)Zsu}/Igs2⁺; Tg(Pbsn-cre)4Prb/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 * FVB/N

endocrine/exocrine glands

increased prostate gland adenocarcinoma incidence ( J:284956 )

♂ • mice develop aggressive adenocarcinomas that occur with much higher frequency than in single Ctnnb1^tm1Mmt conditional mutants, developing prostatic invasive adenocarcinomas as early as 7 months of age

♂ • 4 of 4 mice show intracystic adenocarcinoma at 6-9 months of age, with 1 of 4 mice showing invasive adenocarcinoma

♂ • 13 of 13 mice show intracystic adenocarcinoma at 9 months or older, with 5 of 13 showing invasive adenocarcinoma

increased prostate intraepithelial neoplasia incidence ( J:284956 )

♂ • mice develop PIN lesions starting at 4-6 weeks of age, with 5 of 5 mice showing high grade PIN before 6 months of age

♂ • mice develop more severe PIN lesions and faster disease progression than single Ctnnb1^tm1Mmt conditional mutants

♂ • lesions in the anterior, dorsal, and lateral prostate lobes are more severe than in the ventral prostate

♂ • typical cribriform and papilliferous structures completely fill the lumen of prostatic glands

neoplasm

increased prostate gland adenocarcinoma incidence ( J:284956 )

♂ • mice develop aggressive adenocarcinomas that occur with much higher frequency than in single Ctnnb1^tm1Mmt conditional mutants, developing prostatic invasive adenocarcinomas as early as 7 months of age

♂ • 4 of 4 mice show intracystic adenocarcinoma at 6-9 months of age, with 1 of 4 mice showing invasive adenocarcinoma

♂ • 13 of 13 mice show intracystic adenocarcinoma at 9 months or older, with 5 of 13 showing invasive adenocarcinoma

increased prostate intraepithelial neoplasia incidence ( J:284956 )

♂ • mice develop PIN lesions starting at 4-6 weeks of age, with 5 of 5 mice showing high grade PIN before 6 months of age

♂ • mice develop more severe PIN lesions and faster disease progression than single Ctnnb1^tm1Mmt conditional mutants

♂ • lesions in the anterior, dorsal, and lateral prostate lobes are more severe than in the ventral prostate

♂ • typical cribriform and papilliferous structures completely fill the lumen of prostatic glands

reproductive system

increased prostate gland adenocarcinoma incidence ( J:284956 )

♂ • mice develop aggressive adenocarcinomas that occur with much higher frequency than in single Ctnnb1^tm1Mmt conditional mutants, developing prostatic invasive adenocarcinomas as early as 7 months of age

♂ • 4 of 4 mice show intracystic adenocarcinoma at 6-9 months of age, with 1 of 4 mice showing invasive adenocarcinoma

♂ • 13 of 13 mice show intracystic adenocarcinoma at 9 months or older, with 5 of 13 showing invasive adenocarcinoma

increased prostate intraepithelial neoplasia incidence ( J:284956 )

♂ • mice develop PIN lesions starting at 4-6 weeks of age, with 5 of 5 mice showing high grade PIN before 6 months of age

♂ • mice develop more severe PIN lesions and faster disease progression than single Ctnnb1^tm1Mmt conditional mutants

♂ • lesions in the anterior, dorsal, and lateral prostate lobes are more severe than in the ventral prostate

♂ • typical cribriform and papilliferous structures completely fill the lumen of prostatic glands

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
prostate cancer		DOID:10283	OMIM:176807 OMIM:300147 OMIM:300704 OMIM:601518 OMIM:602759 OMIM:608656 OMIM:608658 OMIM:609299 OMIM:609558 OMIM:610321 OMIM:610997 OMIM:611100 OMIM:611868 OMIM:611928 OMIM:611955 OMIM:611958 OMIM:611959	J:284956

Genotype
MGI:6358667

cn34

• Allelic Composition: Ctnnb1^tm2Kem/Ctnnb1⁺; Nanos3^tm2(cre)Ysa/Nanos3⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6NCrlj * CBA/JNCrlj

cellular

decreased spermatogonia number ( J:257319 )

♂ • reduced number of Rarg+ undifferentiated spermatogonia in tubules

endocrine/exocrine glands

abnormal seminiferous tubule morphology ( J:257319 )

♂ • significantly increased frequency of defective tubules (with lost or exiguous germ cell layer(s))

♂ • significantly increased frequency of Sertoli cell only tubules

♂ • reduced number of Rarg+ undifferentiated spermatogonia in tubules

decreased testis weight ( J:257319 )

♂

reproductive system

decreased spermatogonia number ( J:257319 )

♂ • reduced number of Rarg+ undifferentiated spermatogonia in tubules

abnormal seminiferous tubule morphology ( J:257319 )

♂ • significantly increased frequency of defective tubules (with lost or exiguous germ cell layer(s))

♂ • significantly increased frequency of Sertoli cell only tubules

♂ • reduced number of Rarg+ undifferentiated spermatogonia in tubules

decreased testis weight ( J:257319 )

♂

Genotype
MGI:5581945

cn35

• Allelic Composition: Ctnnb1^tm2Kem/Ctnnb1⁺; Ctsk^tm1(cre)Ska/Ctsk⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6NCrlj * CBA/JNCrlj

skeleton

increased osteoclast cell number ( J:178340 )

decreased trabecular bone volume ( J:178340 )

osteoporosis ( J:178340 )

increased bone resorption ( J:178340 )

hematopoietic system

increased osteoclast cell number ( J:178340 )

immune system

increased osteoclast cell number ( J:178340 )

Genotype
MGI:5581948

cn36

• Allelic Composition: Ctnnb1^tm2Kem/Ctnnb1⁺; Tg(Tek-cre)1Ywa/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

skeleton

increased osteoclast cell number ( J:178340 )

decreased trabecular bone volume ( J:178340 )

osteoporosis ( J:178340 )

increased bone resorption ( J:178340 )

hematopoietic system

increased osteoclast cell number ( J:178340 )

immune system

increased osteoclast cell number ( J:178340 )

Genotype
MGI:3701505

cn37

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Mx1-cre)1Cgn/0
• Genetic Background: involves: 129S1/Sv * C57BL/6 * CBA

mortality/aging

premature death ( J:112659 )

• mice die within 14-18 days of final injection of polyI:polyC used to induce transgene expression and subsequent Ctnnb1 deletion; no treated controls die

skeleton

abnormal trabecular bone morphology ( J:112659 )

• some induced mice show disrupted bone architecture with enhanced trabecular bone structures

neoplasm

increased hepatoblastoma incidence ( J:112659 )

• some induced mutants display hepatoblastoma

integument

skin fibrosis ( J:112659 )

• some induced mice display skin fibrosis

liver/biliary system

increased hepatoblastoma incidence ( J:112659 )

• some induced mutants display hepatoblastoma

Genotype
MGI:4941746

cn38

• Allelic Composition: Amhr2^tm3(cre)Bhr/Amhr2⁺; Ctnnb1^tm1Mmt/Ctnnb1⁺; Pten^tm1Hwu/Pten^tm1Hwu
• Genetic Background: involves: 129S4/SvJae * 129S7/SvEvBrd * 129X1/SvJ

neoplasm

increased ovary tumor incidence ( J:142150 )

♀ • presence of nests of dysplastic cells are seen in the ovaries of newborn mice and E20.5, but not E18.5, indicating that tumor growth begins perinatally

increased granulosa cell tumor incidence ( J:149060 )

• females develop ovarian granulosa cell bilateral tumors with 100% penetrance from an early age

increased testis tumor incidence ( J:149060 )

♂ • 100% penetrance of aggressive testicular cancer

♂ • tumors are first observable at 5 weeks of age, and by 3 months of age, about 70% of mice have unilateral testicular tumors and 30% have bilateral tumors

♂ • tumors exhibit characteristics of granulosa cell tumors of the testis and not Sertoli cell tumors

increased metastatic potential ( J:142150 , J:149060 )

• metastasis is not observed, but this might be that mice do not have sufficient time to develop metastasis due to early lethality, however, when granulosa cell tumors are removed at 6 weeks of age, mice show development of large lung metastases 6-16 weeks later, indicating that tumors indeed are metastatic (J:142150)

• 44% of mice develop pulmonary metastases by 4 months (J:149060)

reproductive system

increased ovary tumor incidence ( J:142150 )

♀ • presence of nests of dysplastic cells are seen in the ovaries of newborn mice and E20.5, but not E18.5, indicating that tumor growth begins perinatally

increased granulosa cell tumor incidence ( J:149060 )

• females develop ovarian granulosa cell bilateral tumors with 100% penetrance from an early age

seminiferous tubule degeneration ( J:149060 )

♂ • seminiferous tubule degeneration is seen by 3 weeks of age

increased testis tumor incidence ( J:149060 )

♂ • 100% penetrance of aggressive testicular cancer

♂ • tumors are first observable at 5 weeks of age, and by 3 months of age, about 70% of mice have unilateral testicular tumors and 30% have bilateral tumors

♂ • tumors exhibit characteristics of granulosa cell tumors of the testis and not Sertoli cell tumors

endocrine/exocrine glands

increased ovary tumor incidence ( J:142150 )

♀ • presence of nests of dysplastic cells are seen in the ovaries of newborn mice and E20.5, but not E18.5, indicating that tumor growth begins perinatally

increased granulosa cell tumor incidence ( J:149060 )

• females develop ovarian granulosa cell bilateral tumors with 100% penetrance from an early age

seminiferous tubule degeneration ( J:149060 )

♂ • seminiferous tubule degeneration is seen by 3 weeks of age

increased testis tumor incidence ( J:149060 )

♂ • 100% penetrance of aggressive testicular cancer

♂ • tumors are first observable at 5 weeks of age, and by 3 months of age, about 70% of mice have unilateral testicular tumors and 30% have bilateral tumors

♂ • tumors exhibit characteristics of granulosa cell tumors of the testis and not Sertoli cell tumors

cardiovascular system

pulmonary embolism ( J:142150 )

• pulmonary tumor cell embolisms

hematopoietic system

extramedullary hematopoiesis ( J:142150 )

• extrensive extramedullary hematopoiesis

anemia ( J:142150 )

• severe anemia

decreased hematocrit ( J:142150 )

mortality/aging

premature death ( J:142150 )

• female mice die before 9 weeks of age

respiratory system

pulmonary embolism ( J:142150 )

• pulmonary tumor cell embolisms

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
granulosa cell tumor		DOID:2999		J:142150
testicular granulosa cell tumor		DOID:5331		J:149060

Genotype
MGI:5432231

cn39

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Kras^tm4Tyj/Kras⁺; Amhr2^tm3(cre)Bhr/Amhr2⁺
• Genetic Background: involves: 129S4/SvJae * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6

neoplasm

increased granulosa cell tumor incidence ( J:186144 )

♀ • female mutants develop granulosa cell tumors by 12-14 weeks of age

increased testis tumor incidence ( J:186144 )

♂ • male mutants develop granulosa cell tumors of the testis by 4-5 months of age; tumors do not spread or metastasize

reproductive system

increased granulosa cell tumor incidence ( J:186144 )

♀ • female mutants develop granulosa cell tumors by 12-14 weeks of age

seminiferous tubule degeneration ( J:186144 )

♂ • seminiferous tubule degeneration is seen by 4 weeks of age

increased testis tumor incidence ( J:186144 )

♂ • male mutants develop granulosa cell tumors of the testis by 4-5 months of age; tumors do not spread or metastasize

endocrine/exocrine glands

increased granulosa cell tumor incidence ( J:186144 )

♀ • female mutants develop granulosa cell tumors by 12-14 weeks of age

seminiferous tubule degeneration ( J:186144 )

♂ • seminiferous tubule degeneration is seen by 4 weeks of age

increased testis tumor incidence ( J:186144 )

♂ • male mutants develop granulosa cell tumors of the testis by 4-5 months of age; tumors do not spread or metastasize

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
granulosa cell tumor		DOID:2999		J:186144
juvenile type testicular granulosa cell tumor		DOID:6032		J:186144
ovarian cancer		DOID:2394	OMIM:167000 OMIM:607893	J:186144

Genotype
MGI:5432232

cn40

• Allelic Composition: Amhr2^tm3(cre)Bhr/Amhr2⁺; Ctnnb1^tm1Mmt/Ctnnb1⁺; Pten^tm1Hwu/Pten^tm1Hwu
• Genetic Background: involves: 129S4/SvJae * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6

neoplasm

increased granulosa cell tumor incidence ( J:186144 )

♀ • female mutants develop granulosa cell tumors by 3 weeks of age

increased testis tumor incidence ( J:186144 )

♂ • male mutants develop testicular granulosa cell tumors by 5 weeks of age

endocrine/exocrine glands

increased granulosa cell tumor incidence ( J:186144 )

♀ • female mutants develop granulosa cell tumors by 3 weeks of age

increased testis tumor incidence ( J:186144 )

♂ • male mutants develop testicular granulosa cell tumors by 5 weeks of age

reproductive system

increased granulosa cell tumor incidence ( J:186144 )

♀ • female mutants develop granulosa cell tumors by 3 weeks of age

increased testis tumor incidence ( J:186144 )

♂ • male mutants develop testicular granulosa cell tumors by 5 weeks of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
granulosa cell tumor		DOID:2999		J:186144
juvenile type testicular granulosa cell tumor		DOID:6032		J:186144
ovarian cancer		DOID:2394	OMIM:167000 OMIM:607893	J:186144

Genotype
MGI:5432224

cn41

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Kras^tm4Tyj/Kras⁺; Tg(CYP19A1-cre)1Jri/0
• Genetic Background: involves: 129S4/SvJae * 129X1/SvJ * C57BL/6

mortality/aging

premature death ( J:186144 )

• mutants die within 3.5-5.5 months of age

neoplasm

increased ovary tumor incidence ( J:186144 )

♀ • female mutants exhibit precancerous lesions in the ovaries at between 4 and 5 weeks of age

increased granulosa cell tumor incidence ( J:186144 )

♀ • female mutants develop bilateral granulosa cell tumors by 3 months of age

endocrine/exocrine glands

impaired granulosa cell differentiation ( J:186144 )

♀ • marker analysis indicates that at 6 weeks of age granulosa cell differentiation is blocked

increased ovary tumor incidence ( J:186144 )

♀ • female mutants exhibit precancerous lesions in the ovaries at between 4 and 5 weeks of age

increased granulosa cell tumor incidence ( J:186144 )

♀ • female mutants develop bilateral granulosa cell tumors by 3 months of age

reproductive system

impaired granulosa cell differentiation ( J:186144 )

♀ • marker analysis indicates that at 6 weeks of age granulosa cell differentiation is blocked

increased ovary tumor incidence ( J:186144 )

♀ • female mutants exhibit precancerous lesions in the ovaries at between 4 and 5 weeks of age

increased granulosa cell tumor incidence ( J:186144 )

♀ • female mutants develop bilateral granulosa cell tumors by 3 months of age

homeostasis/metabolism

decreased circulating estradiol level ( J:186144 )

♀ • at 6 weeks of age in females

increased circulating follicle stimulating hormone level ( J:186144 )

♀ • at 6 weeks of age in females

increased circulating luteinizing hormone level ( J:186144 )

♀ • at 6 weeks of age in females

decreased circulating progesterone level ( J:186144 )

♀ • at 6 weeks of age in females

cellular

impaired granulosa cell differentiation ( J:186144 )

♀ • marker analysis indicates that at 6 weeks of age granulosa cell differentiation is blocked

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
granulosa cell tumor		DOID:2999		J:186144
ovarian cancer		DOID:2394	OMIM:167000 OMIM:607893	J:186144

Genotype
MGI:5432226

cn42

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Pten^tm1Hwu/Pten^tm1Hwu; Tg(CYP19A1-cre)1Jri/0
• Genetic Background: involves: 129S4/SvJae * 129X1/SvJ * C57BL/6

mortality/aging

decreased tumor-free survival time ( J:186144 )

• all mutants die within 2-3 months of age due to tumor burden

neoplasm

increased ovary tumor incidence ( J:186144 )

♀ • mutants exhibit precancerous lesions in the ovaries by 3 weeks of age

increased granulosa cell tumor incidence ( J:186144 )

♀ • mutants develop large granulosa cell tumors by 6-8 weeks of age

endocrine/exocrine glands

decreased granulosa cell apoptosis ( J:186144 )

♀ • granulosa cell apoptosis is decreased in the ovaries at 5-6 weeks of age

impaired granulosa cell differentiation ( J:186144 )

♀ • marker analysis indicates that at 6 weeks of age granulosa cell differentiation is blocked

increased granulosa cell proliferation ( J:186144 )

♀ • granulosa cell proliferation is increased in the ovaries at 5-6 weeks of age

increased ovary tumor incidence ( J:186144 )

♀ • mutants exhibit precancerous lesions in the ovaries by 3 weeks of age

increased granulosa cell tumor incidence ( J:186144 )

♀ • mutants develop large granulosa cell tumors by 6-8 weeks of age

reproductive system

decreased granulosa cell apoptosis ( J:186144 )

♀ • granulosa cell apoptosis is decreased in the ovaries at 5-6 weeks of age

impaired granulosa cell differentiation ( J:186144 )

♀ • marker analysis indicates that at 6 weeks of age granulosa cell differentiation is blocked

increased granulosa cell proliferation ( J:186144 )

♀ • granulosa cell proliferation is increased in the ovaries at 5-6 weeks of age

increased ovary tumor incidence ( J:186144 )

♀ • mutants exhibit precancerous lesions in the ovaries by 3 weeks of age

increased granulosa cell tumor incidence ( J:186144 )

♀ • mutants develop large granulosa cell tumors by 6-8 weeks of age

homeostasis/metabolism

decreased circulating estradiol level ( J:186144 )

• by 6 weeks of age

increased circulating follicle stimulating hormone level ( J:186144 )

• by 6 weeks of age

increased circulating luteinizing hormone level ( J:186144 )

• by 6 weeks of age

decreased circulating progesterone level ( J:186144 )

• by 6 weeks of age

cellular

decreased granulosa cell apoptosis ( J:186144 )

♀ • granulosa cell apoptosis is decreased in the ovaries at 5-6 weeks of age

impaired granulosa cell differentiation ( J:186144 )

♀ • marker analysis indicates that at 6 weeks of age granulosa cell differentiation is blocked

increased granulosa cell proliferation ( J:186144 )

♀ • granulosa cell proliferation is increased in the ovaries at 5-6 weeks of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
granulosa cell tumor		DOID:2999		J:186144
ovarian cancer		DOID:2394	OMIM:167000 OMIM:607893	J:186144

Genotype
MGI:5141743

cn43

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Kras^tm4Tyj/Kras⁺; Tg(Upk2-cre)6Xrw/0
• Genetic Background: involves: 129S4/SvJae * 129X1/SvJ * FVB/N

neoplasm

increased lung tumor incidence ( J:174242 )

respiratory system

increased lung tumor incidence ( J:174242 )

Genotype
MGI:4943270

cn44

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Pten^tm1Hwu/Pten^tm1Hwu; Tg(Upk2-cre)6Xrw/0
• Genetic Background: involves: 129S4/SvJae * 129X1/SvJ * FVB/N

mortality/aging

premature death ( J:164579 )

neoplasm

increased urinary bladder carcinoma incidence ( J:164579 )

• mice develop urothelial bladder tumors that progress to papillary carcinoma

renal/urinary system

increased urinary bladder carcinoma incidence ( J:164579 )

• mice develop urothelial bladder tumors that progress to papillary carcinoma

Genotype
MGI:3830626

cn45

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Prom1^{tm1(cre/ERT2)Gilb}/Prom1⁺
• Genetic Background: involves: 129S6/SvEvTac * 129X1/SvJ

mortality/aging

premature death ( J:144215 )

• tamoxifen administration leads to death of the mouse within 90 days from small intestine carcinoma

neoplasm

increased intestinal adenocarcinoma incidence ( J:144215 )

• two days after tamoxifen administration, there is a marked expansion of YFP⁺ cells within the crypts of the small intestine

• cultures of these cells yields four times as many, and much larger, clonogenic colonies

• ten days after tamoxifen administration, small intestine crypts are markedly disorganized with contiguous streams of YFP⁺ flowing out to the villi and forming a carpet of hyperplastic and grossly dysplastic cells

• sixty days after tamoxifen administration, the small intestine is twice the normal width and has a thickened, rugous appearance

• high-grade intraepithelial neoplasia and crypt adenoma formation is observed at the microscopic level sixty days after tamoxifen administration

• all mice die from the intestinal adenocarcinoma within 90 days of tamoxifen administration

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:144215 )

• two days after tamoxifen administration, there is a marked expansion of YFP⁺ cells within the crypts of the small intestine

• cultures of these cells yields four times as many, and much larger, clonogenic colonies

• ten days after tamoxifen administration, small intestine crypts are markedly disorganized with contiguous streams of YFP⁺ flowing out to the villi and forming a carpet of hyperplastic and grossly dysplastic cells

• sixty days after tamoxifen administration, the small intestine is twice the normal width and has a thickened, rugous appearance

• high-grade intraepithelial neoplasia and crypt adenoma formation is observed at the microscopic level sixty days after tamoxifen administration

• all mice die from the intestinal adenocarcinoma within 90 days of tamoxifen administration

Genotype
MGI:5141741

cn46

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Fgfr3^tm4Cxd/Fgfr3⁺; Tg(Upk2-cre)6Xrw/0
• Genetic Background: involves: 129S6/SvEvTac * 129X1/SvJ * FVB/N

mortality/aging

premature death ( J:174242 )

• shorter survival due to lung cancer, with a survival time between 200-400 days

renal/urinary system

abnormal urinary bladder urothelium morphology ( J:174242 )

• 100% of mutants exhibit areas of hyperproliferation in the bladder urothelium from about 3 months of age, however these lesions do not progress further when examined at 12 months of age

neoplasm

neoplasm ( J:174242 )

N • despite hyperproliferation in the bladder, mutants do not develop urothelial carcinoma by 12 months of age

N • mutants do not develop skin papillomas

increased lung tumor incidence ( J:174242 )

• 36% of mutants develop lung tumors by 1 year of age

• lung tumors resemble solitary fibrous tumors of the lugs (hemangiopericytomas)

respiratory system

increased lung tumor incidence ( J:174242 )

• 36% of mutants develop lung tumors by 1 year of age

• lung tumors resemble solitary fibrous tumors of the lugs (hemangiopericytomas)

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
lung cancer		DOID:1324	OMIM:211980 OMIM:608935 OMIM:612571 OMIM:612593 OMIM:614210	J:174242

Genotype
MGI:5432228

cn47

• Allelic Composition: Amhr2^tm3(cre)Bhr/Amhr2⁺; Ctnnb1^tm1Mmt/Ctnnb1⁺
• Genetic Background: involves: 129S7/SvEvBrd * 129X1/SvJ * C57BL/6

endocrine/exocrine glands

increased granulosa cell tumor incidence ( J:186144 )

♀ • female mutants develop granulosa cell tumors by 6 months of age

seminiferous tubule degeneration ( J:186144 )

♂ • seminiferous tubule degeneration is seen by 5 weeks of age

testicular atrophy ( J:186144 )

♂ • progressive loss of spermatogenesis and testicular atrophy with reduced testis size

increased testis tumor incidence ( J:186144 )

♂ • male mutants develop granulosa cell tumors of the testis by 9-13 weeks of age

reproductive system

increased granulosa cell tumor incidence ( J:186144 )

♀ • female mutants develop granulosa cell tumors by 6 months of age

seminiferous tubule degeneration ( J:186144 )

♂ • seminiferous tubule degeneration is seen by 5 weeks of age

testicular atrophy ( J:186144 )

♂ • progressive loss of spermatogenesis and testicular atrophy with reduced testis size

increased testis tumor incidence ( J:186144 )

♂ • male mutants develop granulosa cell tumors of the testis by 9-13 weeks of age

male infertility ( J:186144 )

♂

neoplasm

increased granulosa cell tumor incidence ( J:186144 )

♀ • female mutants develop granulosa cell tumors by 6 months of age

increased testis tumor incidence ( J:186144 )

♂ • male mutants develop granulosa cell tumors of the testis by 9-13 weeks of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
granulosa cell tumor		DOID:2999		J:186144
ovarian cancer		DOID:2394	OMIM:167000 OMIM:607893	J:186144

Genotype
MGI:3795284

cn48

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Rspo1^tm1Mcch/Rspo1^tm1Mcch; Tg(Nr5a1-cre)5Asc/?
• Genetic Background: involves: 129/Sv * C57BL/6 * CBA

mortality/aging

embryonic lethality, incomplete penetrance ( J:133933 )

• majority of embryos die during early embryonic development due to extensive Beta-catenin activation

reproductive system

reproductive system phenotype ( J:133933 )

N • female mice that survive to birth have a normal reproductive system without the masculinazation of genitalia normally associated with Rspo1 null mice

Genotype
MGI:2673253

cn49

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Pou3f4-cre)32Cren/?
• Genetic Background: involves: 129X1/SvJ

nervous system

abnormal nervous system morphology ( J:83935 )

• increased proliferation of cells by E10

• 110% at E11 to 300% at E11.5

• E11 proliferation rate increased 1.4X

• 6.7% increase in progenitor cell death and apoptosis

• lower proportion of differentiated neurons to proliferative cells

abnormal brain morphology ( J:83935 )

increased brain size ( J:83935 )

• changes similar to those seen in the spinal cord

• tissue mass of the midbrain was increased

• increased proliferation in all areas of the brain

• progenitor domains of the midbrain and other areas of the brain increased

• increased apoptosis

increased spinal cord size ( J:83935 )

• enlarged ventricular zone at E10.5

• increased area occupied by neural progenitor cells

• smaller area occupied by differentiated neurons (as determined immunohistochemically and by activity of genes expressed in progenitor cells)

Genotype
MGI:3045411

cn50

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Col2a1-cre)1Bhr/0
• Genetic Background: involves: 129X1/SvJ

mortality/aging

lethality throughout fetal growth and development, incomplete penetrance ( J:90567 )

• died around E18.5; only 30% survived after birth

skeleton

decreased length of long bones ( J:90567 )

• endochondral bone elements all shorter

Genotype
MGI:2673888

cn51

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Fabp1-cre)1Mmt/?
• Genetic Background: involves: 129X1/SvJ

mortality/aging

premature death ( J:58367 )

• die by 4-5 weeks of age of unknown causes

neoplasm

increased intestinal adenoma incidence ( J:58367 )

• 200-700 intestinal polyps per mouse by 4 weeks of age

digestive/alimentary system

increased intestinal adenoma incidence ( J:58367 )

• 200-700 intestinal polyps per mouse by 4 weeks of age

Genotype
MGI:2673257

cn52

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Krt19^tm1(cre)Mmt/Krt19⁺
• Genetic Background: involves: 129X1/SvJ

mortality/aging

premature death ( J:58367 )

• died around 3 months of age of anemia and cachexia

neoplasm

increased intestinal adenoma incidence ( J:58367 )

• more than 3000 intestinal polyps/mouse by 3 weeks of age

• primarily in the duodenum and proximal jejunum

• lower densities in the ileum

• microadenomas in the colon

digestive/alimentary system

increased intestinal adenoma incidence ( J:58367 )

• more than 3000 intestinal polyps/mouse by 3 weeks of age

• primarily in the duodenum and proximal jejunum

• lower densities in the ileum

• microadenomas in the colon

Genotype
MGI:5475208

cn53

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Dclk1^{tm1.1(cre/ERT2)Seno}/Dclk1⁺
• Genetic Background: involves: 129X1/SvJ * C57BL/6

neoplasm

neoplasm ( J:193873 )

N • 40 days after tamoxifen treatment, mice show no detectable polyp development in the small intestine

Genotype
MGI:4887452

cn54

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Tcfap2a-cre)1Will/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6

mortality/aging

lethality throughout fetal growth and development, incomplete penetrance ( J:168016 )

• most embryos die between E12.5 and 16.5, likely due to vasculature defects

embryonic lethality during organogenesis, incomplete penetrance ( J:168016 )

• most embryos die between E12.5 and 16.5, likely due to vasculature defects

craniofacial

abnormal Meckel's cartilage morphology ( J:168016 )

• in some mutants this is turned downward and in others, is duplicated on the interior aspect

abnormal mandibular prominence morphology ( J:168016 )

• mandibular prominences is increased in size, resulting in lack of proper lower jaw formation or fusion and forming a widened oral cavity

abnormal maxillary prominence morphology ( J:168016 )

• maxillary prominence is increased in size, resulting in lack of proper upper jaw formation or fusion and forming a widened oral cavity

abnormal medial nasal prominence morphology ( J:168016 )

• the nasal process does not show controlled directional growth that results in formation of a normal nasal pit

abnormal facial morphology ( J:168016 )

• most mutants lack any recognizable facial features; some embryos have discernible features but these show severe defects

abnormal face development ( J:168016 )

• embryos do not exhibit recognizable facial features except for a widened oral cavity

• facial development is normal at E9.0, but soon after facial prominences enlarge more rapidly than wild-type

• no significant changes in cell death or proliferation are detected at E10.5

abnormal oral cavity morphology ( J:168016 )

• widened oral cavity

absent outer ear ( J:168016 )

• at E12.5, mutants lack external (visible) ears

skeleton

abnormal Meckel's cartilage morphology ( J:168016 )

• in some mutants this is turned downward and in others, is duplicated on the interior aspect

abnormal cartilage development ( J:168016 )

• cartilages in the head such as the parachordal plate and cartilages of the ear are grossly malformed

• nasal cartilages are wider and misshapen

ectopic cartilage ( J:168016 )

• mutants have extensive ectopic cartilages in the head region resulting in cartilage fusions and malformations

hearing/vestibular/ear

absent outer ear ( J:168016 )

• at E12.5, mutants lack external (visible) ears

vision/eye

abnormal eye morphology ( J:168016 )

• at E12.5, mutants lack external eyes although rudimentary eyes are found internalized

integument

absent vibrissae ( J:168016 )

• at E12.5, mutants lack vibrissae

growth/size/body

abnormal facial morphology ( J:168016 )

• most mutants lack any recognizable facial features; some embryos have discernible features but these show severe defects

abnormal face development ( J:168016 )

• embryos do not exhibit recognizable facial features except for a widened oral cavity

• facial development is normal at E9.0, but soon after facial prominences enlarge more rapidly than wild-type

• no significant changes in cell death or proliferation are detected at E10.5

abnormal oral cavity morphology ( J:168016 )

• widened oral cavity

absent outer ear ( J:168016 )

• at E12.5, mutants lack external (visible) ears

Genotype
MGI:5432223

cn55

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(CYP19A1-cre)1Jri/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6

mortality/aging

premature death ( J:186144 )

• mutants die within 6-8 months of age

neoplasm

increased ovary tumor incidence ( J:186144 )

♀ • ovaries exhibit visible precancerous lesions between 4 and 6 weeks of age and develop granulosa cell tumors

increased granulosa cell tumor incidence ( J:186144 )

reproductive system

increased ovary tumor incidence ( J:186144 )

♀ • ovaries exhibit visible precancerous lesions between 4 and 6 weeks of age and develop granulosa cell tumors

increased granulosa cell tumor incidence ( J:186144 )

endocrine/exocrine glands

increased ovary tumor incidence ( J:186144 )

♀ • ovaries exhibit visible precancerous lesions between 4 and 6 weeks of age and develop granulosa cell tumors

increased granulosa cell tumor incidence ( J:186144 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
ovarian cancer		DOID:2394	OMIM:167000 OMIM:607893	J:186144

Genotype
MGI:5289781

cn56

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Hoxb7-cre)13Amc/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6

Kidney agenesis in Ctnnb1^tm1Mmt/Ctnnb1⁺ Tg(Hoxb7-cre)13Amc/0 mice

renal/urinary system

abnormal kidney development ( J:160547 )

• mice exhit both uni- and bilateral kidney agenesis, similar to that observed in Lrp4^tm2Her homozygotes

• however, formation of the Wolffian duct and distal ureters as well as bladder and adrenal glands remain intact

absent kidney ( J:160547 )

single kidney ( J:160547 )

Genotype
MGI:3836579

cn57

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Pbsn-cre)4Prb/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6 * DBA/2

mortality/aging

premature death ( J:143034 )

• at 428 days

reproductive system

squamous metaplasia of preputial gland ( J:143034 )

• keratinized squamous metaplasia of the preputial gland develops at 100 days (67% incidence), 200 days and at end-point (100% incidence)

squamous metaplasia of bulbourethral gland ( J:143034 )

♂ • mice exhibit keratinized squamous metaplasia in the bulbourethral gland with incidence of 67% at 100 days and 100% at 200 days unlike wild-type mice

increased prostate gland adenocarcinoma incidence ( J:143034 , J:284956 )

♂ • at 200 days, mice develop adenocarcinoma foci (J:143034)

♂ • at end-point, 100% of mice develop diffuse and locally invasive adenocarcinoma unlike wild-type mice (J:143034)

♂ • prostatic tumor tissues show changes consistent with prostatic intracystic adenocarcinomas (J:284956)

♂ • 3 of 5 mice show intracystic adenocarcinoma at 6-9 months of age (J:284956)

♂ • 9 of 12 mice show intracystic adenocarcinoma at 9 months or older, with 1 of 12 showing invasive adenocarcinoma (J:284956)

increased prostate intraepithelial neoplasia incidence ( J:143034 , J:284956 )

♂ • at 100 days, mice exhibit diffuse prostate intraepithelial neoplasia-like keratinized squamous metaplasia unlike in wild-type mice (J:143034)

♂ • at 200 days, mice exhibit high-grade prostate intraepithelial neoplasia-like keratinized squamous metaplasia unlike in wild-type mice (J:143034)

♂ • mice develop PIN lesions starting at 4-6 weeks of age (J:284956)

♂ • 4 of 4 mice develop low grade PIN before 6 months of age and 3 of 4 mice show high grade PIN before 6 months of age (J:284956)

♂ • 5 of 5 mice develop high grade PIN at 6-9 months of age (J:284956)

neoplasm

increased prostate gland adenocarcinoma incidence ( J:143034 , J:284956 )

♂ • at 200 days, mice develop adenocarcinoma foci (J:143034)

♂ • at end-point, 100% of mice develop diffuse and locally invasive adenocarcinoma unlike wild-type mice (J:143034)

♂ • prostatic tumor tissues show changes consistent with prostatic intracystic adenocarcinomas (J:284956)

♂ • 3 of 5 mice show intracystic adenocarcinoma at 6-9 months of age (J:284956)

♂ • 9 of 12 mice show intracystic adenocarcinoma at 9 months or older, with 1 of 12 showing invasive adenocarcinoma (J:284956)

increased prostate intraepithelial neoplasia incidence ( J:143034 , J:284956 )

♂ • at 100 days, mice exhibit diffuse prostate intraepithelial neoplasia-like keratinized squamous metaplasia unlike in wild-type mice (J:143034)

♂ • at 200 days, mice exhibit high-grade prostate intraepithelial neoplasia-like keratinized squamous metaplasia unlike in wild-type mice (J:143034)

♂ • mice develop PIN lesions starting at 4-6 weeks of age (J:284956)

♂ • 4 of 4 mice develop low grade PIN before 6 months of age and 3 of 4 mice show high grade PIN before 6 months of age (J:284956)

♂ • 5 of 5 mice develop high grade PIN at 6-9 months of age (J:284956)

renal/urinary system

squamous metaplasia of urethral gland ( J:143034 )

• urethral keratinized squamous metaplasia develops in 17% at day 200 and 28% at end-points unlike in wild-type mice

endocrine/exocrine glands

squamous metaplasia of preputial gland ( J:143034 )

• keratinized squamous metaplasia of the preputial gland develops at 100 days (67% incidence), 200 days and at end-point (100% incidence)

squamous metaplasia of bulbourethral gland ( J:143034 )

♂ • mice exhibit keratinized squamous metaplasia in the bulbourethral gland with incidence of 67% at 100 days and 100% at 200 days unlike wild-type mice

increased prostate gland adenocarcinoma incidence ( J:143034 , J:284956 )

♂ • at 200 days, mice develop adenocarcinoma foci (J:143034)

♂ • at end-point, 100% of mice develop diffuse and locally invasive adenocarcinoma unlike wild-type mice (J:143034)

♂ • prostatic tumor tissues show changes consistent with prostatic intracystic adenocarcinomas (J:284956)

♂ • 3 of 5 mice show intracystic adenocarcinoma at 6-9 months of age (J:284956)

♂ • 9 of 12 mice show intracystic adenocarcinoma at 9 months or older, with 1 of 12 showing invasive adenocarcinoma (J:284956)

increased prostate intraepithelial neoplasia incidence ( J:143034 , J:284956 )

♂ • at 100 days, mice exhibit diffuse prostate intraepithelial neoplasia-like keratinized squamous metaplasia unlike in wild-type mice (J:143034)

♂ • at 200 days, mice exhibit high-grade prostate intraepithelial neoplasia-like keratinized squamous metaplasia unlike in wild-type mice (J:143034)

♂ • mice develop PIN lesions starting at 4-6 weeks of age (J:284956)

♂ • 4 of 4 mice develop low grade PIN before 6 months of age and 3 of 4 mice show high grade PIN before 6 months of age (J:284956)

♂ • 5 of 5 mice develop high grade PIN at 6-9 months of age (J:284956)

squamous metaplasia of urethral gland ( J:143034 )

• urethral keratinized squamous metaplasia develops in 17% at day 200 and 28% at end-points unlike in wild-type mice

integument

squamous metaplasia of preputial gland ( J:143034 )

• keratinized squamous metaplasia of the preputial gland develops at 100 days (67% incidence), 200 days and at end-point (100% incidence)

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
prostate cancer		DOID:10283	OMIM:176807 OMIM:300147 OMIM:300704 OMIM:601518 OMIM:602759 OMIM:608656 OMIM:608658 OMIM:609299 OMIM:609558 OMIM:610321 OMIM:610997 OMIM:611100 OMIM:611868 OMIM:611928 OMIM:611955 OMIM:611958 OMIM:611959	J:143034

Genotype
MGI:6358659

cn58

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Nanos3^tm2(cre)Ysa/Nanos3⁺
• Genetic Background: involves: 129X1/SvJ * C57BL/6J * C57BL/6NCrlj * CBA/JNCrlj

cellular

decreased spermatogonia number ( J:257319 )

♂ • normal number of Rarg+ undifferentiated spermatogonia in tubules

♂ • significantly reduced number of Gfra1+ undifferentiated spermatogonia in tubules

endocrine/exocrine glands

abnormal seminiferous tubule morphology ( J:257319 )

♂ • significantly increased frequency of defective tubules (with lost or exiguous germ cell layer(s))

♂ • normal number of Rarg+ undifferentiated spermatogonia in tubules

♂ • significantly reduced number of Gfra1+ undifferentiated spermatogonia in tubules

reproductive system

decreased spermatogonia number ( J:257319 )

♂ • normal number of Rarg+ undifferentiated spermatogonia in tubules

♂ • significantly reduced number of Gfra1+ undifferentiated spermatogonia in tubules

abnormal seminiferous tubule morphology ( J:257319 )

♂ • significantly increased frequency of defective tubules (with lost or exiguous germ cell layer(s))

♂ • normal number of Rarg+ undifferentiated spermatogonia in tubules

♂ • significantly reduced number of Gfra1+ undifferentiated spermatogonia in tubules

Genotype
MGI:5581953

cn59

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Ctsk^tm1(cre)Ska/Ctsk⁺
• Genetic Background: involves: 129X1/SvJ * C57BL/6NCrlj * CBA/JNCrlj

skeleton

skeleton phenotype ( J:178340 )

N • mice exhibit normal bone formation

abnormal osteoclast differentiation ( J:178340 )

• impaired

increased bone volume ( J:178340 )

decreased bone resorption ( J:178340 )

hematopoietic system

abnormal osteoclast differentiation ( J:178340 )

• impaired

decreased bone marrow cell number ( J:178340 )

cellular

abnormal osteoclast differentiation ( J:178340 )

• impaired

immune system

abnormal osteoclast differentiation ( J:178340 )

• impaired

Genotype
MGI:5581955

cn60

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Tek-cre)1Ywa/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6 * SJL

mortality/aging

embryonic lethality, complete penetrance ( J:178340 )

Genotype
MGI:3689416

cn61

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
• Genetic Background: involves: 129X1/SvJ * CD-1

mortality/aging

perinatal lethality, complete penetrance ( J:114494 )

• mutants die at birth

limbs/digits/tail

short limbs ( J:114494 )

• from E14.5 - P0, examination shows that limbs are shorter than in wild-type

skeleton

abnormal osteoblast differentiation ( J:114494 )

• expansion of Osx1 expression (Osx1-expressing cells) at E14.5, indicating promotion of osteoblast development, is observed

• no Oc+ terminal osteoblasts are found prior to E16.5, and few that are observed are restricted to periosteal region

abnormal osteoclast differentiation ( J:114494 )

• at E16.5, osteoclasts are absent from mutants when they are detected normally in wild-type

abnormal long bone epiphyseal plate morphology ( J:114494 )

• at E14.5 and 16.5, tibia has abnormal wedge-shaped growth plate with few identifiable hypertrophic chondrocytes visible compared to wild-type

abnormal trabecular bone morphology ( J:114494 )

• at E16.5, no primary spongiosa-like matrix is observed in mutants, unlike wild-type; matrix resembles dense matrix restricted to region forming bone collar

abnormal bone ossification ( J:114494 )

• at E16.5, long bones appear to have a more intense and broader ossification center than in wild-type

• at P0, a thick bony matrix characterizes all long bones; bone formation is apparent in several cranial regions

• at E14.5, osteoblast lineage is expanded and 3-fold increase in proliferation of osteoblast-forming regions along the length of the periosteum

premature endochondral bone ossification ( J:114494 )

• at E14.5, extensive premature bone ossification of the tibia is seen, while no mineralization in wild-type has occurred

delayed intramembranous bone ossification ( J:114494 )

• delayed ossification in skull bones is apparent at E16.5

hematopoietic system

abnormal osteoclast differentiation ( J:114494 )

• at E16.5, osteoclasts are absent from mutants when they are detected normally in wild-type

immune system

abnormal osteoclast differentiation ( J:114494 )

• at E16.5, osteoclasts are absent from mutants when they are detected normally in wild-type

cellular

abnormal osteoblast differentiation ( J:114494 )

• expansion of Osx1 expression (Osx1-expressing cells) at E14.5, indicating promotion of osteoblast development, is observed

• no Oc+ terminal osteoblasts are found prior to E16.5, and few that are observed are restricted to periosteal region

abnormal osteoclast differentiation ( J:114494 )

• at E16.5, osteoclasts are absent from mutants when they are detected normally in wild-type

Genotype
MGI:5319652

cn62

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Col1a1-cre)1Kry/0
• Genetic Background: involves: 129X1/SvJ * FVB

mortality/aging

lethality at weaning, complete penetrance ( J:98430 )

• normal for the first two weeks after birth but die within a few days after weaning

craniofacial

absent lower incisors ( J:98430 )

• form but fail to erupt

skeleton

absent lower incisors ( J:98430 )

• form but fail to erupt

decreased osteoclast cell number ( J:98430 )

increased osteoma incidence ( J:98430 )

• benign tumors in the ribs of 80% of mice

increased bone mass ( J:98430 )

neoplasm

increased osteoma incidence ( J:98430 )

• benign tumors in the ribs of 80% of mice

hematopoietic system

decreased osteoclast cell number ( J:98430 )

immune system

decreased osteoclast cell number ( J:98430 )

growth/size/body

absent lower incisors ( J:98430 )

• form but fail to erupt

Genotype
MGI:4943264

cn63

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Upk2-cre)6Xrw/0
• Genetic Background: involves: 129X1/SvJ * FVB/N

renal/urinary system

abnormal urinary bladder urothelium morphology ( J:164579 , J:174242 )

• mice develop hyperplastic lesions in the bladder unlike wild-type mice (J:164579)

• 100% of mutants exhibit areas of hyperproliferation in the bladder urothelium from about 3 months of age, however these lesions do not progress further when examined at 12 months of age (J:174242)

neoplasm

neoplasm ( J:164579 , J:174242 )

N • hyperproliferative lesions in the bladder do not progress to carcinoma (J:164579)

N • mutants aged up to 18 months do not develop lung tumors, skin tumors or urothelial carcinoma (J:174242)

Genotype
MGI:5428002

cn64

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tg(Cdh16-cre)91Igr/0
• Genetic Background: involves: 129X1/SvJ * ICR

mortality/aging

postnatal lethality, complete penetrance ( J:151498 )

• mice die by P2

renal/urinary system

kidney cyst ( J:151498 )

dilated renal tubule ( J:151498 )

• mild at birth

growth/size/body

kidney cyst ( J:151498 )

Genotype
MGI:5428001

cn65

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Wnt9b^tm1.1Amc/Wnt9b^tm1.2Amc; Tg(Cdh16-cre)91Igr/0
• Genetic Background: involves: 129X1/SvJ * ICR

renal/urinary system

kidney cyst ( J:151498 )

• cystic index at P1 is increased compared to in Wnt9b^tm1.1Amc/Wnt9b^tm1.2Amc Tg(Cdh16-cre)91Igr mice

growth/size/body

kidney cyst ( J:151498 )

• cystic index at P1 is increased compared to in Wnt9b^tm1.1Amc/Wnt9b^tm1.2Amc Tg(Cdh16-cre)91Igr mice

Genotype
MGI:4947311

cx66

• Allelic Composition: Ctnnb1^Bfc/Ctnnb1⁺; Dkk1^tm1Lmgd/Dkk1⁺; Lrp6^Gw/Lrp6⁺
• Genetic Background: either: (involves: 101/H * 129 * BALB/cCrl * C3H) or (involves: 101/H * 129 * BALB/cCrl * C3H * C57BL/6)

embryo

caudal body truncation ( J:170646 )

• 23% of mice exhibit complete head truncation unlike wild-type mice

growth/size/body

abnormal head size ( J:170646 )

• all mice exhibit head reduction defects unlike wild-type mice

Genotype
MGI:4947310

cx67

• Allelic Composition: Ctnnb1^Bfc/Ctnnb1⁺; Lrp6^Gw/Lrp6⁺
• Genetic Background: either: (involves: 101/H * BALB/cCrl * C3H) or (involves: 101/H * BALB/cCrl * C3H * C57BL/6)

growth/size/body

abnormal head size ( J:170646 )

• 86% of mice exhibit head reduction defects unlike wild-type mice

Genotype
MGI:4947312

cx68

• Allelic Composition: Ctnnb1^Bfc/Ctnnb1⁺; Dkk1^tm1Lmgd/Dkk1⁺
• Genetic Background: either: (involves: 129/Sv * BALB/cCrl * C3H/HeNCrl) or (involves: 129/Sv * BALB/cCrl * C3H/HeNCrl * C57BL/6)

mortality/aging

preweaning lethality, incomplete penetrance ( J:170646 )

• fewer than expected mice are produced

• viability is less than in Ctnnb1^Bfc heterozygotes

vision/eye

abnormal eye morphology ( J:170646 )

• ocular defects are higher than in Ctnnb1^Bfc heterozygotes

growth/size/body

abnormal head morphology ( J:170646 )

• 92% of mice exhibit head defects compared with wild-type mice

• head defects are higher than in Ctnnb1^Bfc heterozygotes

Genotype
MGI:4429576

cx69

• Allelic Composition: Apc^tm1Tno/Apc^tm1Tno; Ctnnb1^tm4.1Wbm/Ctnnb1⁺
• Genetic Background: involves: 129 * 129P2/OlaHsd * 129S4/SvJae * C57BL/6

neoplasm

decreased tumor incidence ( J:156864 )

• no mutant mice (n=8) develope hepatocellular carcinomas by 450 days of age

Genotype
MGI:4429574

cx70

• Allelic Composition: Apc^Min/Apc^tm1Tno; Ctnnb1^tm4.1Wbm/Ctnnb1⁺
• Genetic Background: involves: 129 * 129P2/OlaHsd * 129S4/SvJae * C57BL/6

Anterior head defects during embryonic development in Apc^Min/Apc^tm1Tno embryos and rescue of head defects by Ctnnb1^tm4.1Wbm/Ctnnb1⁺

liver/biliary system

increased hepatocellular carcinoma incidence ( J:156864 )

• hepatocellular carcinomas (HCC) in 47% of mutant mice (n=15), including 20% that showed intestinal comorbidity

• mice only have HCC (n=4) live longer than Apc^min/+ mice

nervous system

nervous system phenotype ( J:156864 )

N • normal head morphology

craniofacial

craniofacial phenotype ( J:156864 )

N • normal head morphology

digestive/alimentary system

intestine polyps ( J:156864 )

• reduced tumor multiplicity and incidence, leaving 6 of 15 mice (40%) free of polyps

• the remaining macroscopic lesions are of tubulo-villous structure

• similar size and latency to those observed in age-matched Apc^min/+ mice

neoplasm

increased hepatocellular carcinoma incidence ( J:156864 )

• hepatocellular carcinomas (HCC) in 47% of mutant mice (n=15), including 20% that showed intestinal comorbidity

• mice only have HCC (n=4) live longer than Apc^min/+ mice

Genotype
MGI:4429575

cx71

• Allelic Composition: Apc^Min/Apc^Min; Ctnnb1^tm4.1Wbm/Ctnnb1⁺
• Genetic Background: involves: 129 * 129P2/OlaHsd * C57BL/6

mortality/aging

embryonic lethality between implantation and somite formation, complete penetrance ( J:156864 )

• death immediately after gastrulation

• embryos only detected at embryonic day 4.5 (E4.5) and E5.5 but not at later stages (E6 and E7)

Genotype
MGI:5314535

cx72

• Allelic Composition: Ctnnb1^tm1Max/Ctnnb1⁺; Hesx1^tm1(cre)Jpmb/Hesx1^tm1Icar
• Genetic Background: involves: 129P2/OlaHsd * 129S * 129X1/SvJ * C57BL/6

nervous system

abnormal forebrain development ( J:181005 )

small embryonic telencephalon ( J:181005 )

• in some mice

vision/eye

microphthalmia ( J:181005 )

• bilateral in some mice

• unilateral in some mice

anophthalmia ( J:181005 )

• unilateral in some mice

Genotype
MGI:5314538

cx73

• Allelic Composition: Ctnnb1^tm1Max/Ctnnb1⁺; Hesx1^tm1Icar/Hesx1^tm1Icar
• Genetic Background: involves: 129P2/OlaHsd * 129S * 129X1/SvJ * C57BL/6

nervous system

abnormal forebrain development ( J:181005 )

small embryonic telencephalon ( J:181005 )

• in some mice

vision/eye

microphthalmia ( J:181005 )

• bilateral in some mice

• unilateral in some mice

anophthalmia ( J:181005 )

• unilateral in some mice

Genotype
MGI:5319651

cx74

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Tcf7^tm1Cle/Tcf7⁺
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ

skeleton

abnormal bone structure ( J:98430 )

• very low bone density

Genotype
MGI:5430611

cx75

• Allelic Composition: Apc^tm2Rfo/Apc⁺; Ctnnb1^tm1.2Wvv/Ctnnb1⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

embryonic lethality, complete penetrance ( J:185942 )

embryo

rostral body truncation ( J:185942 )

• anterior truncation

Genotype
MGI:5430610

cx76

• Allelic Composition: Apc^tm1Rak/Apc⁺; Ctnnb1^tm1.2Wvv/Ctnnb1⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

embryonic lethality, complete penetrance ( J:185942 )

embryo

rostral body truncation ( J:185942 )

• anterior truncation

nervous system

abnormal telencephalon development ( J:185942 )

• severe reduction in the telencephalic region of the brain

Genotype
MGI:3809920

cx77

• Allelic Composition: Ctnnb1^tm2.1Kem/Ctnnb1⁺; Sall4^{Gt(W097E01)Flo}/Sall4⁺
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6

mortality/aging

preweaning lethality, complete penetrance ( J:138922 )

• absent at weaning possibly indicating embryonic lethality

embryo

abnormal mesoderm development ( J:138922 )

• expression analysis indicates impaired mesoderm development

embryonic growth retardation ( J:138922 )

• at E7.5

abnormal anterior primitive streak morphology ( J:138922 )

• a gap in T expression is seen in the anterior primitive streak between E7.5 and E7.75 in the area where cells fate mapped to give rise to paraxial mesoderm are found

growth/size/body

embryonic growth retardation ( J:138922 )

• at E7.5

Genotype
MGI:3840269

cx78

• Allelic Composition: Axin1^tm4Cos/Axin1^tm4Cos; Ctnnb1^tm2.1Kem/Ctnnb1⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * FVB/N

mortality/aging

mortality/aging ( J:147293 )

N • unlike Axin1^tm4Cos homozygotes, mice survive until E18.5 when they are sacrificed

craniofacial

abnormal facial morphology ( J:147293 )

cleft palate ( J:147293 )

abnormal nose morphology ( J:147293 )

• mice lack nasal structures unlike wild-type mice

respiratory system

abnormal nose morphology ( J:147293 )

• mice lack nasal structures unlike wild-type mice

nervous system

abnormal brain morphology ( J:147293 )

• mice have multiple brain malformations unlike wild-type mice

digestive/alimentary system

cleft palate ( J:147293 )

growth/size/body

abnormal head morphology ( J:147293 )

abnormal facial morphology ( J:147293 )

cleft palate ( J:147293 )

abnormal nose morphology ( J:147293 )

• mice lack nasal structures unlike wild-type mice

Genotype
MGI:3612484

cx79

• Allelic Composition: Ctnnb1^tm2.1Kem/Ctnnb1⁺; Otx2^{tm1(Dkk1)Imat}/Otx2^{tm1(Dkk1)Imat}
• Genetic Background: involves: 129/Sv * C57BL/6 * CBA

embryo

abnormal rostral-caudal axis patterning ( J:103272 )

• based on expression of anterior visceral endoderm markers, the anterior migration defects of distal visceral endoderm cells observed in 6.5 p.d.c. Otx2^tm2/Otx2^tm2 embryo was partially rescued