Phenotypes associated with this allele

• Allele Symbol: Gt(ROSA)26Sor^tm1(EYFP)Cos
• Allele Name: targeted mutation 1, Frank Costantini
• Allele ID: MGI:2449038
• Summary: 51 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Runx1^tm2.1(cre/Esr1*)Ims/Runx1^tm1Medv	B6.Cg-Gt(ROSA)26Sor^tm1(EYFP)Cos Runx1^tm2.1(cre/Esr1*)Ims	MGI:5316038
cn2	Ascl1^tm1And/Ascl1^tm1And Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Tg(Ascl1-EGFP,-cre)1Jejo/0	involves: 129 * 129X1/SvJ * C57BL/6 * DBA	MGI:4420909
cn3	Nkx6-1^tm1Jlr/Nkx6-1^tm1.1Msan Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Tg(Ins2-cre)25Mgn/0	involves: 129 * C57BL/6 * DBA * SJL	MGI:5501188
cn4	Rbpj^tm1Hon/Rbpj^tm1.1Hon Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Ptf1a^tm2(cre/ESR1)Cvw/Ptf1a^+	involves: 129P2/OlaHsd * 129S1/Sv * 129S6/SvEvTac	MGI:5310800
cn5	Rbpj^tm1Hon/Rbpj^tm1.1Hon Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Hes1^tm1(cre/ERT2)Lcm/Hes1^+	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ	MGI:5310799
cn6	Cd9^tm1c(EUCOMM)Hmgu/Cd9^tm1c(EUCOMM)Hmgu Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Kras^tm4Tyj/Kras^+ Tg(Pdx1-cre)6Tuv/0 Trp53^tm1Brn/Trp53^+	involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N	MGI:6377668
cn7	Cd9^tm1c(EUCOMM)Hmgu/Cd9^+ Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Kras^tm4Tyj/Kras^+ Tg(Pdx1-cre)6Tuv/0 Trp53^tm1Brn/Trp53^tm1Brn	involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N	MGI:6377665
cn8	Cd9^tm1c(EUCOMM)Hmgu/Cd9^+ Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Kras^tm4Tyj/Kras^+ Tg(Pdx1-cre)6Tuv/0 Trp53^tm1Brn/Trp53^+	involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N	MGI:6377664
cn9	Cd9^tm1c(EUCOMM)Hmgu/Cd9^tm1c(EUCOMM)Hmgu Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Kras^tm4Tyj/Kras^+ Tg(Pdx1-cre)6Tuv/0 Trp53^tm1Brn/Trp53^tm1Brn	involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N	MGI:6377669
cn10	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Kras^tm4Tyj/Kras^+ Tg(Pdx1-cre)6Tuv/0 Trp53^tm1Brn/Trp53^tm1Brn	involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * FVB/N	MGI:6377672
cn11	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Kras^tm4Tyj/Kras^+ Tg(Pdx1-cre)6Tuv/0 Trp53^tm1Brn/Trp53^+	involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * FVB/N	MGI:6377671
cn12	Myo18a^tm1c(KOMP)Wtsi/Myo18a^tm1c(KOMP)Wtsi Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Lyz2^tm1(cre)Ifo/Lyz2^+	involves: 129P2/OlaHsd * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6N	MGI:6360589
cn13	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Ighg1^tm1(cre)Cgn/Ighg1^+ Prdm1^tm2Masu/Prdm1^tm2Masu	involves: 129P2/OlaHsd * 129X1/SvJ	MGI:5762939
cn14	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Lhx6^tm2Vpa/Lhx6^tm2Vpa Tg(Nkx2-1-cre)1Wdr/0	involves: 129P2/OlaHsd * 129X1/SvJ	MGI:5491493
cn15	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Cd19^tm1(cre)Cgn/Cd19^+ Rev3l^tm1.1Diaz/Rev3l^tm1.1Diaz	involves: 129P2/OlaHsd * 129X1/SvJ * BALB/c * C57BL/6 * C57BL/6NTac	MGI:5442608
cn16	Cdc42^tm1Brak/Cdc42^tm1Brak Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Lgr5^tm1(cre/ERT2)Cle/Lgr5^+	involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6	MGI:5427870
cn17	Syk^tm1.1(cre)Fkfr/Syk^tm1.1(cre)Fkfr Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^tm1(EYFP)Cos	involves: 129S1/Sv * 129X1/SvJ	MGI:4844099
cn18	Lcp2^tm1Gak/Lcp2^tm2Gak Tg(VAV1-cre)1Graf/0 Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+	involves: 129S1/Sv * 129X1/SvJ	MGI:4843965
cn19	Eed^tm1Sho/Eed^tm1Sho Epor^tm1.1(EGFP/icre)Uk/Epor^+ Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^tm1(EYFP)Cos	involves: 129S1/Sv * 129X1/SvJ * BALB/cJ	MGI:4410547
cn20	Lcp2^tm1Gak/Lcp2^tm2Gak Tg(Pf4-icre)Q3Rsko/0 Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:4843964
cn21	Ednrb^tm1Nrd/Ednrb^tm1Nrd Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ H2az2^Tg(Wnt1-cre)11Rth/H2az2^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA/J	MGI:3814191
cn22	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Ilk^tm1Star/Ilk^tm1Star Tg(Krt1-15-cre/PGR*)22Cot/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL/J	MGI:5009342
cn23	Fev^tm1Esd/Fev^tm2Esd Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Tg(Fev-cre)1Esd/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:4837213
cn24	Ctnnb1^tm2Kem/Ctnnb1^tm2.1Kem Corin^tm2(cre)Bamo/Corin^+ Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+	involves: 129S1/Sv * 129X1/SvJ * FVB/N	MGI:4844104
cn25	Hoxb1^tm1Mist/Hoxb1^tm1Mist Tg(Hoxb1-cre)r4Mist/0 Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+	involves: 129S2/SvPas * 129X1/SvJ * C57BL/6 * CD-1	MGI:5491185
cn26	Hoxb1^tm1.1Mist/Hoxb1^tm1.1Mist Tg(Hoxb1-cre)r4Mist/0 Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+	involves: 129S2/SvPas * 129X1/SvJ * C57BL/6 * CD-1	MGI:5491188
cn27	Col1a1^tm1(tetO-EWSR1/ATF1)Yasu/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(EYFP)Cos Tg(Mpz-cre)94Imeg/0	involves: 129S4/SvJae * 129X1/SvJ * C57BL/6	MGI:5485201
cn28	Myo18a^tm1c(KOMP)Wtsi/Myo18a^tm1c(KOMP)Wtsi Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Tg(Tnnt2-cre)5Blh/0	involves: 129S4/SvJaeSor * 129X1/SvJ * C57BL/6 * C57BL/6N * DBA/2	MGI:6360587
cn29	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
cn30	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ S1pr1^tm2Rlp/S1pr1^tm2Rlp Tg(Cdh5-cre/ERT2)1Rha/0	involves: 129S6/SvEvTac * 129X1/SvJ	MGI:5445987
cn31	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^tm1(EYFP)Cos Pax7^tm1(cre/ERT2)Gaka/Pax7^tm1(cre/ERT2)Gaka Paxbp1^tm1.1Nju/Paxbp1^tm1.1Nju	involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6NCr	MGI:6827448
cn32	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Rest^tm1.1Jhsi/Rest^tm1.1Jhsi Tg(Nes-cre/ERT2)KEisc/0	involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * SJL	MGI:5141116
cn33	Sh2d1a^tm1.1Knic/Sh2d1a^tm1.1Knic Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Ndor1^Tg(UBC-cre/ERT2)1Ejb/0	involves: 129S/SvEv * 129X1/SvJ * C57BL/6	MGI:5502763
cn34	Sh2d1a^tm1.1Knic/Y Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Ndor1^Tg(UBC-cre/ERT2)1Ejb/0	involves: 129S/SvEv * 129X1/SvJ * C57BL/6	MGI:5502766
cn35	Pdpk1^tm1.1Mlw/Pdpk1^tm1.1Mlw Rag2^tm1Fwa/Rag2^tm1Fwa Tnfrsf4^tm2(cre)Nik/Tnfrsf4^+ Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+	involves: 129S/SvEv * 129X1/SvJ * C57BL/6	MGI:5697630
cn36	Slc17a6^tm1.1Thna/Slc17a6^tm1.1Thna Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Slc6a3^tm1(cre)Xz/Slc6a3^+	involves: 129/Sv * 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6J	MGI:4879095
cn37	Bhlhe22^tm3.1(cre)Meg/Bhlhe22^tm1Meg Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+	involves: 129/Sv * 129X1/SvJ	MGI:4440935
cn38	Cd79a^tm1(cre)Reth/Cd79a^+ Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+	involves: 129X1/SvJ * BALB/c * C57BL/6	MGI:3687456
cn39	Gt(ROSA)26Sor^tm1Hjf/Gt(ROSA)26Sor^tm1(EYFP)Cos Tg(CMV-cre)1Cgn/0	involves: 129X1/SvJ * BALB/cJ * C57BL/6	MGI:3696483
cn40	Pdpk1^tm1.1Mlw/Pdpk1^tm1.1Mlw Tnfrsf4^tm2(cre)Nik/Tnfrsf4^+ Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+	involves: 129X1/SvJ * C57BL/6	MGI:5697628
cn41	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Hprt1^tm1(Ins2-HBEGF)Herr/Y Tg(Gcg-rtTA)#Herr/0 Tg(tetO-cre)1Jaw/0	involves: 129X1/SvJ * C57BL/6	MGI:5567830
cn42	Amotl1^tm1Laho/Amotl1^tm1Laho Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Tg(Cdh5-cre/ERT2)1Rha/0	involves: 129X1/SvJ * C57BL/6	MGI:6723729
cn43	Ctdnep1^tm3Ryn/Ctdnep1^tm3Ryn Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Six2^tm1(tTA,tetO-EGFP/cre)Amc/Six2^+	involves: 129X1/SvJ * C57BL/6 * C57BL/6J	MGI:5548193
cn44	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Hprt1^tm1(Ins2-HBEGF)Herr/Y Tg(Ins2-cre/ERT)1Dam/0	involves: 129X1/SvJ * C57BL/6 * CBA	MGI:5567828
cn45	Bcl11a^tm1Pwt/Bcl11a^tm1Pwt Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Tg(Mx1-cre)1Cgn/0	involves: 129X1/SvJ * C57BL/6 * CBA	MGI:5564909
cn46	Gt(ROSA)26Sor^tm1(EYFP)Cos/? Tg(Il17f-cre)1Awai/?	involves: 129X1/SvJ * C57BL/6 * DBA	MGI:3831109
cn47	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Plcg1^tm1Gcrp/Plcg1^tm1Rwen Tg(Cd4-cre)1Cwi/0	involves: 129X1/SvJ * C57BL/6 * DBA/2	MGI:4437914
cn48	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Il22^tm1.1(icre)Stck/Il22^+	involves: 129X1/SvJ * C57BL/6N	MGI:5634193
cn49	Gt(ROSA)26Sor^tm1(EYFP)Cos/? Tg(Lck-cre)548Jxm/0	involves: 129X1/SvJ * C57BL/6 * SJL	MGI:3696478
cn50	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Tg(Plp1-Ncre)DFki/0 Tg(Plp1-Ccre)RFki/0	involves: 129X1/SvJ * FVB/N	MGI:3835668
cn51	Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^+ Tg(GFAP-Ccre)FFki/0 Tg(GFAP-Ncre)VFki/0	involves: 129X1/SvJ * FVB/N	MGI:3835669

Genotype
MGI:5316038

cn1

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Runx1^{tm2.1(cre/Esr1*)Ims}/Runx1^tm1Medv
• Genetic Background: B6.Cg-Gt(ROSA)26Sor^tm1(EYFP)Cos Runx1^{tm2.1(cre/Esr1*)Ims}

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

hematopoietic system

hematopoietic system phenotype ( J:182232 )

N • with maternal injection of high-dose tamoxifen on E7.5 to induce Runx1 reactivation, trasnsplanted, hematopoietic stem cells were isolated and injected into irradiated recipients for a long-term competitive repopulation assay; at E14.5 and E16.5, no signficant differences in reconstitution levels of hematopoietic cells is observed relative to controls

N • secondary transplantation of yolk sac-derived bone marrow cells from the primary recipients 12 months following primary transplantation resulted in long-term engraftment

abnormal hematopoietic system morphology/development ( J:182232 )

• exposure of embryos to tamoxifen at E10.5 fails to result in observation of CD45+ definitive hematopoietic cells in the aorta-gonad-mesonephros (AGM) region (no rescue of definitive hematopoiesis), whereas after exposure to tamoxifen at E7.5, a large population of CD45-positive cells are detected

Genotype
MGI:4420909

cn2

• Allelic Composition: Ascl1^tm1And/Ascl1^tm1And; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Tg(Ascl1-EGFP,-cre)1Jejo/0
• Genetic Background: involves: 129 * 129X1/SvJ * C57BL/6 * DBA

nervous system

abnormal dorsal interneuron morphology ( J:98830 )

• the precursors to dI3 and dI5 do not leave the ventricular zone at E10.5-E11.5 unlike in controls

• labeled cells do not appear to significantly contribute to the increase in dI2 and dI4 numbers

Genotype
MGI:5501188

cn3

• Allelic Composition: Nkx6-1^tm1Jlr/Nkx6-1^tm1.1Msan; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Tg(Ins2-cre)25Mgn/0
• Genetic Background: involves: 129 * C57BL/6 * DBA * SJL

endocrine/exocrine glands

abnormal pancreatic beta cell differentiation ( J:195153 )

• maintenance of beta cell is impaired with conversion to delta cell fate

decreased pancreatic beta cell number ( J:195153 )

increased pancreatic delta cell number ( J:195153 )

cellular

abnormal pancreatic beta cell differentiation ( J:195153 )

• maintenance of beta cell is impaired with conversion to delta cell fate

Genotype
MGI:5310800

cn4

• Allelic Composition: Rbpj^tm1Hon/Rbpj^tm1.1Hon; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Ptf1a^{tm2(cre/ESR1)Cvw}/Ptf1a⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129S6/SvEvTac

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:180310 )

N • tamoxifen-treated mice exhibit normal proliferation of YFP+ acinar cells

Genotype
MGI:5310799

cn5

• Allelic Composition: Rbpj^tm1Hon/Rbpj^tm1.1Hon; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Hes1^{tm1(cre/ERT2)Lcm}/Hes1⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:180310 )

N • tamoxifen-treated mice exhibit normal pancreatic ductal morphology and pancreata mass

abnormal centroacinar cell of Langerhans morphology ( J:180310 )

• tamoxifen-treated mice exhibit a decrease in YFP+ centroacinar cells compared with control mice

increased pancreatic acinar cell number ( J:180310 )

• tamoxifen-treated mice exhibit an increase in YFP+ acinar cells compared with control mice

abnormal pancreas physiology ( J:180310 )

• tamoxifen-treated mice exhibit a rapid transformation of YFP+ centroacinar cells into acinar cells compared with control mice

• however, tamoxifen-treated mice exhibit normal centroacinar and acinar cells proliferation and apoptosis

digestive/alimentary system

abnormal centroacinar cell of Langerhans morphology ( J:180310 )

• tamoxifen-treated mice exhibit a decrease in YFP+ centroacinar cells compared with control mice

increased pancreatic acinar cell number ( J:180310 )

• tamoxifen-treated mice exhibit an increase in YFP+ acinar cells compared with control mice

Genotype
MGI:6377668

cn6

• Allelic Composition: Cd9^{tm1c(EUCOMM)Hmgu}/Cd9^{tm1c(EUCOMM)Hmgu}; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Kras^tm4Tyj/Kras⁺; Tg(Pdx1-cre)6Tuv/0; Trp53^tm1Brn/Trp53⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N

mortality/aging

premature death ( J:280854 )

• as severe as in mice wild-type for Cd9

neoplasm

increased pancreatic intraepithelial neoplasia incidence ( J:280854 )

• at 8 weeks, more severe than in mice heterozygous for the Cd9 conditional allele

endocrine/exocrine glands

increased pancreatic intraepithelial neoplasia incidence ( J:280854 )

• at 8 weeks, more severe than in mice heterozygous for the Cd9 conditional allele

Genotype
MGI:6377665

cn7

• Allelic Composition: Cd9^{tm1c(EUCOMM)Hmgu}/Cd9⁺; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Kras^tm4Tyj/Kras⁺; Tg(Pdx1-cre)6Tuv/0; Trp53^tm1Brn/Trp53^tm1Brn
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N

mortality/aging

premature death ( J:280854 )

• not as severe as in mice wild-type for Cd9 or homozygous for a conditional allele

Genotype
MGI:6377664

cn8

• Allelic Composition: Cd9^{tm1c(EUCOMM)Hmgu}/Cd9⁺; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Kras^tm4Tyj/Kras⁺; Tg(Pdx1-cre)6Tuv/0; Trp53^tm1Brn/Trp53⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N

mortality/aging

premature death ( J:280854 )

• not as severe as in mice wild-type for Cd9 or homozygous for a conditional allele

neoplasm

increased pancreatic intraepithelial neoplasia incidence ( J:280854 )

• at 8 weeks, not as severe as in mice wild-type for Cd9 or homozygous for a conditional allele

• increased tumor weight compared to in mice homozygous for a conditional allele

decreased tumor growth/size ( J:280854 )

• compared to in mice homozygous for a conditional allele

endocrine/exocrine glands

increased pancreatic intraepithelial neoplasia incidence ( J:280854 )

• at 8 weeks, not as severe as in mice wild-type for Cd9 or homozygous for a conditional allele

• increased tumor weight compared to in mice homozygous for a conditional allele

Genotype
MGI:6377669

cn9

• Allelic Composition: Cd9^{tm1c(EUCOMM)Hmgu}/Cd9^{tm1c(EUCOMM)Hmgu}; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Kras^tm4Tyj/Kras⁺; Tg(Pdx1-cre)6Tuv/0; Trp53^tm1Brn/Trp53^tm1Brn
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N

mortality/aging

premature death ( J:280854 )

• as severe as in mice wild-type for Cd9

Genotype
MGI:6377672

cn10

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Kras^tm4Tyj/Kras⁺; Tg(Pdx1-cre)6Tuv/0; Trp53^tm1Brn/Trp53^tm1Brn
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * FVB/N

mortality/aging

premature death ( J:280854 )

• all mice die by 8 weeks of age

Genotype
MGI:6377671

cn11

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Kras^tm4Tyj/Kras⁺; Tg(Pdx1-cre)6Tuv/0; Trp53^tm1Brn/Trp53⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * FVB/N

mortality/aging

premature death ( J:280854 )

• all mice die by 30 weeks of age

neoplasm

increased pancreatic ductal adenocarcinoma incidence ( J:280854 )

• at 8 weeks

increased pancreatic intraepithelial neoplasia incidence ( J:280854 )

• at 8 weeks

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:280854 )

• at 8 weeks

increased pancreatic intraepithelial neoplasia incidence ( J:280854 )

• at 8 weeks

Genotype
MGI:6360589

cn12

• Allelic Composition: Myo18a^{tm1c(KOMP)Wtsi}/Myo18a^{tm1c(KOMP)Wtsi}; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Lyz2^tm1(cre)Ifo/Lyz2⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6N

immune system

immune system phenotype ( J:277320 )

N • no differences in the morphological polarization, motility, or chemotactic efficiency of macrophages are seen in a complement C5a gradient chemotaxis assay

N • macrophages exhibit normal Golgi morphology

Genotype
MGI:5762939

cn13

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Ighg1^tm1(cre)Cgn/Ighg1⁺; Prdm1^tm2Masu/Prdm1^tm2Masu
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ

hematopoietic system

enlarged spleen ( J:167612 )

• splenomegaly in all terminally ill mice

abnormal plasma cell differentiation ( J:167612 )

• plasma cell formation is severely impeded 10 days after primary and secondary immunization

increased germinal center B cell number ( J:167612 )

• mice show increased numbers of germinal center B cells at day 10 after primary immunizations

abnormal germinal center B cell physiology ( J:167612 )

• small, but significant, increase of the fraction of germinal center B cells in the S and G2 phases of the cell cycle

decreased IgG1 level ( J:167612 )

• reduction in total as well as sheep red blood cell-specific IgG1, but not IgM, antibodies 10 days after primary and secondary immunization

immune system

enlarged spleen ( J:167612 )

• splenomegaly in all terminally ill mice

abnormal plasma cell differentiation ( J:167612 )

• plasma cell formation is severely impeded 10 days after primary and secondary immunization

increased germinal center B cell number ( J:167612 )

• mice show increased numbers of germinal center B cells at day 10 after primary immunizations

abnormal germinal center B cell physiology ( J:167612 )

• small, but significant, increase of the fraction of germinal center B cells in the S and G2 phases of the cell cycle

decreased IgG1 level ( J:167612 )

• reduction in total as well as sheep red blood cell-specific IgG1, but not IgM, antibodies 10 days after primary and secondary immunization

enlarged lymph nodes ( J:167612 )

• occasional lymphadenopathy

liver/biliary system

enlarged liver ( J:167612 )

• hepatomegaly in one mouse

mortality/aging

decreased survivor rate ( J:167612 )

• shortened survival

premature death ( J:167612 )

• shortened survival

neoplasm

increased B cell derived lymphoma incidence ( J:167612 )

• spleens and lymph nodes show presence of large cells with a diffuse growth pattern, resembling diffuse large B cell lymphoma (DLBCL)

• lymphoproliferations are of clonal origin

• 5 of 6 DLBCLs are consistent with activated B cell-DLBCL

growth/size/body

enlarged liver ( J:167612 )

• hepatomegaly in one mouse

enlarged spleen ( J:167612 )

• splenomegaly in all terminally ill mice

Genotype
MGI:5491493

cn14

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Lhx6^tm2Vpa/Lhx6^tm2Vpa; Tg(Nkx2-1-cre)1Wdr/0
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ

nervous system

abnormal brain interneuron morphology ( J:196342 )

• mice exhibit impaired somatostatin+ cortical interneuron differentiation compared with control mice

Genotype
MGI:5442608

cn15

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Cd19^tm1(cre)Cgn/Cd19⁺; Rev3l^tm1.1Diaz/Rev3l^tm1.1Diaz
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ * BALB/c * C57BL/6 * C57BL/6NTac

immune system

immune system phenotype ( J:188723 )

N • mice exhibit normal B cell development in the bone marrow and spleen

decreased B cell proliferation ( J:188723 )

• following with activation LPS, less so when activated with LPS plus IL4

abnormal class switch recombination ( J:188723 )

• following activated with LPS and IL4, mice exhibit decreased IgG1+ cells, indicating reduced class switch recombination, compared with wild-type mice

abnormal somatic hypermutation frequency ( J:188723 )

• following immunization with NP-CGG in alum, splenic B cells exhibit reduced mutation frequency in the rearranged Vh186.2 H chains compared with wild-type cells

• Peyer's patch B cells exhibit reduced accumulation of mutation at the intron downstream of rearranged V genes compared with wild-type cells

hematopoietic system

decreased B cell proliferation ( J:188723 )

• following with activation LPS, less so when activated with LPS plus IL4

abnormal class switch recombination ( J:188723 )

• following activated with LPS and IL4, mice exhibit decreased IgG1+ cells, indicating reduced class switch recombination, compared with wild-type mice

abnormal somatic hypermutation frequency ( J:188723 )

• following immunization with NP-CGG in alum, splenic B cells exhibit reduced mutation frequency in the rearranged Vh186.2 H chains compared with wild-type cells

• Peyer's patch B cells exhibit reduced accumulation of mutation at the intron downstream of rearranged V genes compared with wild-type cells

cellular

decreased B cell proliferation ( J:188723 )

• following with activation LPS, less so when activated with LPS plus IL4

Genotype
MGI:5427870

cn16

• Allelic Composition: Cdc42^tm1Brak/Cdc42^tm1Brak; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Lgr5^{tm1(cre/ERT2)Cle}/Lgr5⁺
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6

digestive/alimentary system

increased small intestinal crypt cell apoptosis ( J:184563 )

• intestinal crypt stem cells show increased cell death following tamoxifen administration

abnormal intestinal epithelium morphology ( J:184563 )

• 3 weeks after tamoxifen administration, mutant villus epithelial cells show disrupted cell polarity, as indicated by disorganized nuclear alignment

• stem cells contribute less to the villus epithelial compartments than in controls following tamoxifen administration

abnormal crypts of Lieberkuhn morphology ( J:184563 )

• 3 weeks after tamoxifen administration, more mutant stem cells in intestinal crypts undergo mitosis compared to control stem cells

• stem cells contribute less to the villus epithelial compartments than in controls following tamoxifen administration, indicating reduced clonal expansion of mutant stem cells

absent Paneth cells ( J:184563 )

• 2 weeks after tamoxifen administration, mutant stem cells in intestinal crypts fail to give rise to Paneth cells

abnormal small intestinal villus morphology ( J:184563 )

• 3 weeks after tamoxifen administration, mutant villus epithelial cells show disrupted cell polarity, as indicated by disorganized nuclear alignment

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:184563 )

• 3 weeks after tamoxifen administration, more mutant stem cells in intestinal crypts undergo mitosis compared to control stem cells

• stem cells contribute less to the villus epithelial compartments than in controls following tamoxifen administration, indicating reduced clonal expansion of mutant stem cells

absent Paneth cells ( J:184563 )

• 2 weeks after tamoxifen administration, mutant stem cells in intestinal crypts fail to give rise to Paneth cells

cellular

increased small intestinal crypt cell apoptosis ( J:184563 )

• intestinal crypt stem cells show increased cell death following tamoxifen administration

Genotype
MGI:4844099

cn17

• Allelic Composition: Syk^{tm1.1(cre)Fkfr}/Syk^{tm1.1(cre)Fkfr}; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^tm1(EYFP)Cos
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

immune system

decreased leukocyte cell number ( J:159112 )

• fetal livers exhibit reduced leukocyte cellularity and colony forming cell frequency compared with wild-type livers

increased leukocyte cell number ( J:159112 )

• at E12.5 and E15.5, abnormal blood vessel morphology is associated with massive leukocyte accumulation

• YFP+ monocyte- or macrophage-like cells accumulate in the skin compared to in Sykb^{tm1.1(cre)Fkfr}/Sykb⁺ Gt(ROSA)26Sor^tm1(EYFP)Cos homozygotes

abnormal lymphangiogenesis ( J:159112 )

liver/biliary system

abnormal liver development ( J:159112 )

• at E13.5, liver development is reduced compared to in wild-type mice

• fetal livers exhibit reduced leukocyte cellularity and colony forming cell frequency compared with wild-type livers

decreased liver weight ( J:159112 )

• at E13.5

liver hypoplasia ( J:159112 )

• at E13.5

cardiovascular system

abnormal blood vessel morphology ( J:159112 )

• at E12.5 and E15.5, abnormal blood vessel morphology is associated with massive leukocyte accumulation

hematopoietic system

decreased leukocyte cell number ( J:159112 )

• fetal livers exhibit reduced leukocyte cellularity and colony forming cell frequency compared with wild-type livers

increased leukocyte cell number ( J:159112 )

• at E12.5 and E15.5, abnormal blood vessel morphology is associated with massive leukocyte accumulation

• YFP+ monocyte- or macrophage-like cells accumulate in the skin compared to in Sykb^{tm1.1(cre)Fkfr}/Sykb⁺ Gt(ROSA)26Sor^tm1(EYFP)Cos homozygotes

Genotype
MGI:4843965

cn18

• Allelic Composition: Lcp2^tm1Gak/Lcp2^tm2Gak; Tg(VAV1-cre)1Graf/0; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

immune system

abnormal lymphatic vessel morphology ( J:162815 )

• at E14.5, mice exhibit blood-filled cutaneous lymphatics unlike in wild-type mice

• neonates exhibit blood-filled mesenteric lymphatics unlike in wild-type mice

digestive/alimentary system

intestinal edema ( J:162815 )

homeostasis/metabolism

intestinal edema ( J:162815 )

Genotype
MGI:4410547

cn19

• Allelic Composition: Eed^tm1Sho/Eed^tm1Sho; Epor^{tm1.1(EGFP/icre)Uk}/Epor⁺; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^tm1(EYFP)Cos
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * BALB/cJ

hematopoietic system

abnormal erythropoiesis ( J:154730 )

• increase in the percentage of cells in the R2 stage (lin-,CD71+,Ter119-) and reduction in the percentage of cells in the R3 stage (lin-,CD71+,Ter119+)

Genotype
MGI:4843964

cn20

• Allelic Composition: Lcp2^tm1Gak/Lcp2^tm2Gak; Tg(Pf4-icre)Q3Rsko/0; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6

immune system

abnormal Peyer's patch morphology ( J:162815 )

• some mice exhibit blood-filled Peyer patches unlike in wild-type mice

abnormal lymphatic vessel morphology ( J:162815 )

• mice exhibit blood-filled mesenteric and intestinal lymphatic vessels unlike wild-type mice

homeostasis/metabolism

abnormal platelet activation ( J:162815 )

• platelets from neonates without vascular phenotypes exhibit intermediate levels of convulxin-stimulated fibrinogen binding compared with similarly treated wild-type cells

hematopoietic system

abnormal platelet activation ( J:162815 )

• platelets from neonates without vascular phenotypes exhibit intermediate levels of convulxin-stimulated fibrinogen binding compared with similarly treated wild-type cells

Genotype
MGI:3814191

cn21

• Allelic Composition: Ednrb^tm1Nrd/Ednrb^tm1Nrd; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; H2az2^{Tg(Wnt1-cre)11Rth}/H2az2⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA/J

mortality/aging

premature death ( J:140320 )

• mice die 5 weeks after birth

growth/size/body

slow postnatal weight gain ( J:140320 )

• after P25

distended abdomen ( J:140320 )

digestive/alimentary system

aganglionic megacolon ( J:140320 )

pigmentation

white spotting ( J:140320 )

• mice lack coat pigment in the trunk

embryo

abnormal enteric neural crest cell migration ( J:140320 )

• enteric neural crest cells fail to reach the anus

integument

white spotting ( J:140320 )

• mice lack coat pigment in the trunk

cellular

abnormal enteric neural crest cell migration ( J:140320 )

• enteric neural crest cells fail to reach the anus

Genotype
MGI:5009342

cn22

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Ilk^tm1Star/Ilk^tm1Star; Tg(Krt1-15-cre/PGR*)22Cot/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL/J

homeostasis/metabolism

abnormal wound healing ( J:172933 )

• during wound regeneration, RU486-treated mice exhibit YFP+ cells in the suprabasal layers but not the basal layers unlike in control mice

delayed wound healing ( J:172933 )

• in RU486-treated mice

integument

abnormal hair follicle development ( J:172933 )

• following treatment with RU486, plated YFP+ hair follicle stem cells do not exhibit spreading unlike YFP- cells

Genotype
MGI:4837213

cn23

• Allelic Composition: Fev^tm1Esd/Fev^tm2Esd; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Tg(Fev-cre)1Esd/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

nervous system

abnormal somatosensory cortex morphology ( J:165266 )

• serotonergic innervation of the somatosensory cortex from dorsal raphe nucleus 5-HT neurons is significantly disrupted

abnormal innervation ( J:165266 )

• serotonergic innervation of the somatosensory cortex from dorsal raphe nucleus 5-HT neurons is significantly disrupted

abnormal serotonergic neuron morphology ( J:165266 )

• serotonergic innervation of the somatosensory cortex from dorsal raphe nucleus 5-HT neurons is significantly disrupted

abnormal nervous system electrophysiology ( J:165266 )

• neither high nor low concentrations of 8-Hydroxy-2-dipropylaminotetralin hydrobromide (8-OH-DPAT) elicit a change in baseline currents in labeled 5HT neurons

abnormal action potential ( J:165266 )

• YFP+ cells show increased spontaneous firing of action potentials

Genotype
MGI:4844104

cn24

• Allelic Composition: Ctnnb1^tm2Kem/Ctnnb1^tm2.1Kem; Corin^tm2(cre)Bamo/Corin⁺; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * FVB/N

integument

abnormal auchene hair morphology ( J:160311 )

• auchene growth is terminated before formation of the single bend unlike in wild-type mice

• however, the first segment is normal

abnormal awl hair morphology ( J:160311 )

• shorter, thinner, and more numerous than in wild-type mice

decreased guard hair length ( J:160311 )

abnormal hair shaft morphology ( J:160311 )

• at the end of the first hair cycle, all hairs are shorter and thinner than in wild-type mice

abnormal zigzag hair morphology ( J:160311 )

• the first segment of zigzag hairs is variable in length from 60% to 100% of wild-type hair length

• the second segment is reduced in length 50% to 60% compared to in wild-type mice

• the first and second segments are thinner than in wild-type mice

• zigzag hairs lack the third and fourth segment unlike in wild-type mice

abnormal hair cycle anagen phase ( J:160311 )

• duration of anagen is decreased compared to in wild-type mice

• hair follicles enter catagen prematurely compared to in wild-type mice

abnormal hair cycle catagen phase ( J:160311 )

• catagen onset occurs at P12 and is less synchronized than in wild-type mice

abnormal hair cycle telogen phase ( J:160311 )

• telogen begins earlier than in wild-type mice

delayed hair regrowth ( J:160311 )

• 40 days after depilation, only sparse hair regenerate unlike in similarly treated wild-type mice

abnormal hair follicle physiology ( J:160311 )

• proliferation of matrix progenitor cells abutting the dermal papilla (MPADs) and their progeny is reduced compared to in wild-type mice

• mice fail to exhibit normal hair follicle regeneration compared with wild-type mice

increased hair follicle apoptosis ( J:160311 )

• the number of apoptotic cells averaged over all follicles is increased

cellular

increased hair follicle apoptosis ( J:160311 )

• the number of apoptotic cells averaged over all follicles is increased

Genotype
MGI:5491185

cn25

• Allelic Composition: Hoxb1^tm1Mist/Hoxb1^tm1Mist; Tg(Hoxb1-cre)r4Mist/0; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S2/SvPas * 129X1/SvJ * C57BL/6 * CD-1

hearing/vestibular/ear

abnormal organ of Corti morphology ( J:197162 )

• very few crossing medial olivocochlear (MOC) terminals are observed contacting outer hair cells in adult mice

abnormal cochlear outer hair cell morphology ( J:197162 )

• at P8, no difference in shape or organization of outer hair cells (OHCs) is observed at the apical and basal turns relative to wild-type

• morphological defects of OHCs in adults are less severe than observed in constitutive Hoxb1-deficient (Hoxb1^tm1.2Fmr) mice but statistically significant loss of OHCs and moderate OHC ciliar malformations are observed

• no abnormalities are observed in basal regions

increased or absent threshold for auditory brainstem response ( J:197162 )

• at 3 months, threshold is pathologically elevated compared to the normal 40dB, but not as significantly as in Hoxb1^tm1.2Fmr (null) mice

• thresholds are elevated at all ages tested (from 1-12 months), increasing progressively to double the control level

increased susceptibility to age-related hearing loss ( J:197162 )

nervous system

abnormal cochlear outer hair cell morphology ( J:197162 )

• at P8, no difference in shape or organization of outer hair cells (OHCs) is observed at the apical and basal turns relative to wild-type

• morphological defects of OHCs in adults are less severe than observed in constitutive Hoxb1-deficient (Hoxb1^tm1.2Fmr) mice but statistically significant loss of OHCs and moderate OHC ciliar malformations are observed

• no abnormalities are observed in basal regions

abnormal brainstem morphology ( J:197162 )

• area of the ventral nucleus of the lateral lemniscus is reduced by about 50% compared to wild-type controls at P8

abnormal pons morphology ( J:197162 )

• specification and innervation of olivocochlear neurons is abnormal, no crossing olivocochlear (MOC) efferent neurons cross the midline at P8

• the cholinergic population of lateral olivocochlear (LOC) neurons is absent indicating defective specification

abnormal cochlear VIII nucleus morphology ( J:197162 )

• axon pathfinding defects are observed, with ectopic r4-derived projections crossing the midline and innervating the medial nucleus of the trapezoid body (MNTB)

Genotype
MGI:5491188

cn26

• Allelic Composition: Hoxb1^tm1.1Mist/Hoxb1^tm1.1Mist; Tg(Hoxb1-cre)r4Mist/0; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S2/SvPas * 129X1/SvJ * C57BL/6 * CD-1

hearing/vestibular/ear

abnormal organ of Corti morphology ( J:197162 )

• very few crossing medial olivocochlear (MOC) terminals are observed contacting outer hair cells in adult mice

abnormal cochlear outer hair cell morphology ( J:197162 )

• at P8, no difference in shape or organization of outer hair cells (OHCs) is observed at the apical and basal turns relative to wild-type, but in adults (3 months), OHC rows are severely disorganized with loss of some hair cells in the apical turn of the cochlea; no inner hair cells (IHCs) are lost

• OHCs in the basal turns show only slight abnormalities in ciliar organization and orientation

increased or absent threshold for auditory brainstem response ( J:197162 )

• at 3 months, threshold is elevated to 90 dB compared to the normal 40dB

• thresholds are elevated at all ages tested (from 1-12 months), increasing progressively to double the control level

abnormal susceptibility to hearing loss ( J:197162 )

• mice raised in acoustic isolation display ABR threshold increases compared to controls, indicating that sensitivity to environmental sounds is not a significant factor

increased susceptibility to age-related hearing loss ( J:197162 )

nervous system

abnormal cochlear outer hair cell morphology ( J:197162 )

• at P8, no difference in shape or organization of outer hair cells (OHCs) is observed at the apical and basal turns relative to wild-type, but in adults (3 months), OHC rows are severely disorganized with loss of some hair cells in the apical turn of the cochlea; no inner hair cells (IHCs) are lost

• OHCs in the basal turns show only slight abnormalities in ciliar organization and orientation

abnormal brainstem morphology ( J:197162 )

• area of the ventral nucleus of the lateral lemniscus is severely reduced by about 90% compared to wild-type controls at P8

abnormal pons morphology ( J:197162 )

• specification and innervation of olivocochlear neurons is abnormal, no medial olivocochlear (MOC) efferent neurons cross the midline at P8

• the cholinergic population of lateral olivocochlear (LOC) neurons is very small indicating defective specification

abnormal cochlear VIII nucleus morphology ( J:197162 )

• axon pathfinding defects are observed, with ectopic r4-derived projections crossing the midline and innervating the medial nucleus of the trapezoid body (MNTB)

Genotype
MGI:5485201

cn27

• Allelic Composition: Col1a1^{tm1(tetO-EWSR1/ATF1)Yasu}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^tm1(EYFP)Cos; Tg(Mpz-cre)94Imeg/0
• Genetic Background: involves: 129S4/SvJae * 129X1/SvJ * C57BL/6

neoplasm

increased sarcoma incidence ( J:194505 )

• in of all doxycycline-treated mice arising from neural crest-lineage cells

Genotype
MGI:6360587

cn28

• Allelic Composition: Myo18a^{tm1c(KOMP)Wtsi}/Myo18a^{tm1c(KOMP)Wtsi}; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Tg(Tnnt2-cre)5Blh/0
• Genetic Background: involves: 129S4/SvJaeSor * 129X1/SvJ * C57BL/6 * C57BL/6N * DBA/2

mortality/aging

lethality throughout fetal growth and development, complete penetrance ( J:277320 )

• no mice are produced and only remnants of embryos are detected at E14.5

Genotype
MGI:3830626

cn29

• 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:5445987

cn30

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; S1pr1^tm2Rlp/S1pr1^tm2Rlp; Tg(Cdh5-cre/ERT2)1Rha/0
• Genetic Background: involves: 129S6/SvEvTac * 129X1/SvJ

cardiovascular system

abnormal aorta morphology ( J:189010 )

• glomeruloid lesions form when tamoxifen is administered throughout pregnancy, although these lesions are less severe than in germ line null mice

abnormal retina vasculature morphology ( J:189010 )

• endothelial hyper-sprouting and retention of mural cell coverage on arteries and veins are detected after tamoxifen treatment

vision/eye

abnormal retina vasculature morphology ( J:189010 )

• endothelial hyper-sprouting and retention of mural cell coverage on arteries and veins are detected after tamoxifen treatment

Genotype
MGI:6827448

cn31

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor^tm1(EYFP)Cos; Pax7^{tm1(cre/ERT2)Gaka}/Pax7^{tm1(cre/ERT2)Gaka}; Paxbp1^tm1.1Nju/Paxbp1^tm1.1Nju
• Genetic Background: involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6NCr

cellular

abnormal mitochondrial morphology ( J:304562 )

• fragmented mitochondria, largely restricted to perinuclear region, lacking interconnecting tubular network in activated muscle stem cells

abnormal respiratory electron transport chain ( J:304562 )

• defective cellular respiration and glycolysis

abnormal mitochondrial ATP synthesis coupled electron transport ( J:304562 )

• defective cellular respiration and glycolysis

decreased mitochondrial fission ( J:304562 )

• defective mitochondrial biogenesis in activated muscle stem cells

abnormal oxidative phosphorylation ( J:304562 )

• defective cellular respiration and glycolysis

muscle

impaired skeletal muscle regeneration ( J:304562 )

• virtual absence of regenerating myofibers 5 days after injection of cardiotoxin (CTX) into the tibialis anterior (TA) muscles and no muscle regeneration after 14 nor 30 days

• adipocyte infiltration 30 days after injection of cardiotoxin (CTX) into the tibialis anterior (TA) muscles

Genotype
MGI:5141116

cn32

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Rest^tm1.1Jhsi/Rest^tm1.1Jhsi; Tg(Nes-cre/ERT2)KEisc/0
• Genetic Background: involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * SJL

nervous system

abnormal neuron differentiation ( J:174056 )

• 20 days after tamoxifen treatment, mice exhibit a transient increase in hippocampal neurogenesis compared with control mice

• tamoxifen-treatment increased hippocampal neurogenesis in vitro and in vivo compared with controls

• tamoxifen-treated mice exhibit premature exit of quiescence compared with control mice

• tamoxifen-treated mice exhibit loss of neurogenic capacity of adult neurospheres and decreased neurogenesis over time compared with control mice

• neurospheres treated from tamoxifen-treated mice exhibit reduced self-renewal capacity compared with wild-type cells

• however, hippocampal neurogenesis is normal 10 and 30 days after tamoxifen treatment

premature neuronal precursor differentiation ( J:174056 )

• in tamoxifen-treated mice

decreased neuron number ( J:174056 )

• tamoxifen-treated mice exhibit decreased adult-generated immature and mature granule neurons compared with control mice

cellular

abnormal neuron differentiation ( J:174056 )

• 20 days after tamoxifen treatment, mice exhibit a transient increase in hippocampal neurogenesis compared with control mice

• tamoxifen-treatment increased hippocampal neurogenesis in vitro and in vivo compared with controls

• tamoxifen-treated mice exhibit premature exit of quiescence compared with control mice

• tamoxifen-treated mice exhibit loss of neurogenic capacity of adult neurospheres and decreased neurogenesis over time compared with control mice

• neurospheres treated from tamoxifen-treated mice exhibit reduced self-renewal capacity compared with wild-type cells

• however, hippocampal neurogenesis is normal 10 and 30 days after tamoxifen treatment

premature neuronal precursor differentiation ( J:174056 )

• in tamoxifen-treated mice

Genotype
MGI:5502763

cn33

• Allelic Composition: Sh2d1a^tm1.1Knic/Sh2d1a^tm1.1Knic; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Ndor1^{Tg(UBC-cre/ERT2)1Ejb}/0
• Genetic Background: involves: 129S/SvEv * 129X1/SvJ * C57BL/6

immune system

immune system phenotype ( J:196692 )

N • tamoxifen-treated mice exhibit normal invariant NKT cell numbers, phenotype and in vivo responsiveness to lipid antigens

abnormal NK T cell physiology ( J:196692 )

• in vitro TCR-induced invariant NKT (iNKT) cell cytotoxicity from tamoxifen-treated mice is impaired compared to in control cells

• iNKT cells from tamoxifen-treated mice exhibit impaired control of tumor growth in vivo compared with control cells

• in response to EL4 targets, iNKT cells from tamoxifen-treated mcie form fewer conjugates and produce reduced levels of cytokines (IFN-gamma and IL4) compared with control cells

• however, iNKT cells exhibit normal trafficking to the tumor site

decreased circulating interleukin-4 level ( J:196692 )

• from iNKT cells from tamoxifen-treated mice in response to EL4 targets

decreased interferon-gamma secretion ( J:196692 )

• from iNKT cells from tamoxifen-treated mice in response to EL4 targets

homeostasis/metabolism

decreased circulating interleukin-4 level ( J:196692 )

• from iNKT cells from tamoxifen-treated mice in response to EL4 targets

hematopoietic system

abnormal NK T cell physiology ( J:196692 )

• in vitro TCR-induced invariant NKT (iNKT) cell cytotoxicity from tamoxifen-treated mice is impaired compared to in control cells

• iNKT cells from tamoxifen-treated mice exhibit impaired control of tumor growth in vivo compared with control cells

• in response to EL4 targets, iNKT cells from tamoxifen-treated mcie form fewer conjugates and produce reduced levels of cytokines (IFN-gamma and IL4) compared with control cells

• however, iNKT cells exhibit normal trafficking to the tumor site

Genotype
MGI:5502766

cn34

• Allelic Composition: Sh2d1a^tm1.1Knic/Y; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Ndor1^{Tg(UBC-cre/ERT2)1Ejb}/0
• Genetic Background: involves: 129S/SvEv * 129X1/SvJ * C57BL/6

immune system

immune system phenotype ( J:196692 )

♂N • tamoxifen-treated mice exhibit normal invariant NKT cell numbers, phenotype and in vivo responsiveness to lipid antigens

abnormal NK T cell physiology ( J:196692 )

♂ • in vitro TCR-induced invariant NKT (iNKT) cell cytotoxicity from tamoxifen-treated mice is impaired compared to in control cells

♂ • iNKT cells from tamoxifen-treated mice exhibit impaired control of tumor growth in vivo compared with control cells

♂ • in response to EL4 targets, iNKT cells from tamoxifen-treated mcie form fewer conjugates and produce reduced levels of cytokines (IFN-gamma and IL4) compared with control cells

♂ • however, iNKT cells exhibit normal trafficking to the tumor site

decreased circulating interleukin-4 level ( J:196692 )

♂ • from iNKT cells from tamoxifen-treated mice in response to EL4 targets

decreased interferon-gamma secretion ( J:196692 )

♂ • from iNKT cells from tamoxifen-treated mice in response to EL4 targets

homeostasis/metabolism

decreased circulating interleukin-4 level ( J:196692 )

♂ • from iNKT cells from tamoxifen-treated mice in response to EL4 targets

hematopoietic system

abnormal NK T cell physiology ( J:196692 )

♂ • in vitro TCR-induced invariant NKT (iNKT) cell cytotoxicity from tamoxifen-treated mice is impaired compared to in control cells

♂ • iNKT cells from tamoxifen-treated mice exhibit impaired control of tumor growth in vivo compared with control cells

♂ • in response to EL4 targets, iNKT cells from tamoxifen-treated mcie form fewer conjugates and produce reduced levels of cytokines (IFN-gamma and IL4) compared with control cells

♂ • however, iNKT cells exhibit normal trafficking to the tumor site

Genotype
MGI:5697630

cn35

• Allelic Composition: Pdpk1^tm1.1Mlw/Pdpk1^tm1.1Mlw; Rag2^tm1Fwa/Rag2^tm1Fwa; Tnfrsf4^tm2(cre)Nik/Tnfrsf4⁺; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S/SvEv * 129X1/SvJ * C57BL/6

mortality/aging

premature death ( J:226194 )

• mice succumb to disease at 12-16 weeks of age

integument

abnormal keratinocyte differentiation ( J:226194 )

• marker analysis indicates impaired keratinocyte differentiation

dermatitis ( J:226194 )

• mice develop mild skin dermatitis

epidermal hyperplasia ( J:226194 )

immune system

dermatitis ( J:226194 )

• mice develop mild skin dermatitis

cellular

abnormal keratinocyte differentiation ( J:226194 )

• marker analysis indicates impaired keratinocyte differentiation

Genotype
MGI:4879095

cn36

• Allelic Composition: Slc17a6^tm1.1Thna/Slc17a6^tm1.1Thna; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Slc6a3^tm1(cre)Xz/Slc6a3⁺
• Genetic Background: involves: 129/Sv * 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6J

nervous system

abnormal dopaminergic neuron morphology ( J:167767 )

• only a minority of dopaminergic projections remain intake

abnormal excitatory postsynaptic currents ( J:167767 )

• YFP+ dopamine neurons fail to exhibit glutamatergic excitatory postsynaptic currents (EPSCs) unlike control cells

• at P9 to P10, mice exhibit a reduction in glutamatergic with fewer neurons responding to ventral tegmental area stimulation compared with similarly treated control cells

behavior/neurological

impaired behavioral response to cocaine ( J:167767 )

• cocaine-treated mice exhibit less locomotor activity compared with control mice

• however, cocaine-treated mice exhibit conditioned place preference

homeostasis/metabolism

decreased dopamine level ( J:167767 )

• the ventral striatum exhibit reduced dopamine and evoked dopamine release compared to in control mice

Genotype
MGI:4440935

cn37

• Allelic Composition: Bhlhe22^{tm3.1(cre)Meg}/Bhlhe22^tm1Meg; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129/Sv * 129X1/SvJ

nervous system

abnormal spinal cord dorsal horn morphology ( J:158273 )

• quantification of neurons at P0 shows a 50% decrease in number of marked neurons in superficial dorsal horn compared to controls with no difference in numbers in any other spinal cord region

• significant increase in number of apoptotic cells (marked neurons) in superficial dorsal horn is observed at E18.5, but no difference is observed at E17.5 or 19.5

• partial loss of glutamatergic and GABAergic neurons is observed in dorsal horn

• number of marked neurons in dorsal horn are not different from controls when BrdU labeling is done at E12.5 or E13.5 and analysis is done at E17.5, indicating that neuronal mitosis is not affected

Genotype
MGI:3687456

cn38

• Allelic Composition: Cd79a^tm1(cre)Reth/Cd79a⁺; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129X1/SvJ * BALB/c * C57BL/6

homeostasis/metabolism

abnormal enzyme/coenzyme activity ( J:113645 )

• 97% of B lineage cells are EYFP-positive compared with 33% in Cd19^tm1(cre)Cgn-expressing mice indicating more efficient loxP recombination in developing B cells

Genotype
MGI:3696483

cn39

• Allelic Composition: Gt(ROSA)26Sor^tm1Hjf/Gt(ROSA)26Sor^tm1(EYFP)Cos; Tg(CMV-cre)1Cgn/0
• Genetic Background: involves: 129X1/SvJ * BALB/cJ * C57BL/6

normal phenotype

no abnormal phenotype detected ( J:117041 )

• analysis of hematopoietic cells demonstrates reliable detection of YFP and RFP in same cells as well as in different cells

Genotype
MGI:5697628

cn40

• Allelic Composition: Pdpk1^tm1.1Mlw/Pdpk1^tm1.1Mlw; Tnfrsf4^tm2(cre)Nik/Tnfrsf4⁺; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129X1/SvJ * C57BL/6

mortality/aging

premature death ( J:226194 )

• mice develop a wasting syndrome and succumb to disease by 11 weeks of age

growth/size/body

cachexia ( J:226194 )

enlarged spleen ( J:226194 )

• mice develop an enlarged spleen

integument

abnormal hypodermis fat layer morphology ( J:226194 )

• loss of hypodermal fat

abnormal keratinocyte differentiation ( J:226194 )

• marker analysis indicates impaired keratinocyte differentiation

impaired skin barrier function ( J:226194 )

• mice with advanced disease show loss of skin barrier integrity at 7-8 weeks of age

dermatitis ( J:226194 )

• mice develop severe, systemic dermatitis starting at 5 weeks of age

• inflammation is not seen in the lung, liver, kidney or gut

premature hair loss ( J:226194 )

• dermatitis is accompanied by hair loss

hair follicle degeneration ( J:226194 )

• loss of hair follicles

hyperkeratosis ( J:226194 )

epidermal hyperplasia ( J:226194 )

• mild epidermal hyperplasia and microabsceess are seen at 3 weeks of age but not at 10 days of age

scaly skin ( J:226194 )

• skin contains epidermal scales

skin lesions ( J:226194 )

• skin of mice with advanced disease contains lesions with epidermal damage, resulting in loss of skin barrier integrity

skin hyperplasia ( J:226194 )

thick skin ( J:226194 )

• dermatitis is accompanied by skin thickening

skin fibrosis ( J:226194 )

• increase in dermal fibrosis

immune system

enlarged spleen ( J:226194 )

• mice develop an enlarged spleen

abnormal regulatory T cell number ( J:226194 )

• decrease in the frequency of Foxp3+ CD25+ Tregs with a corresponding increase in Foxp3-CD25+ effector T cells

abnormal T cell physiology ( J:226194 )

• CD4 T cells exhibit an activated phenotype

• mice develop systemic T helper type 2 immunity

enlarged lymph nodes ( J:226194 )

• mice develop peripheral lymphadenopathy

dermatitis ( J:226194 )

• mice develop severe, systemic dermatitis starting at 5 weeks of age

• inflammation is not seen in the lung, liver, kidney or gut

homeostasis/metabolism

impaired skin barrier function ( J:226194 )

• mice with advanced disease show loss of skin barrier integrity at 7-8 weeks of age

hematopoietic system

enlarged spleen ( J:226194 )

• mice develop an enlarged spleen

abnormal regulatory T cell number ( J:226194 )

• decrease in the frequency of Foxp3+ CD25+ Tregs with a corresponding increase in Foxp3-CD25+ effector T cells

abnormal T cell physiology ( J:226194 )

• CD4 T cells exhibit an activated phenotype

• mice develop systemic T helper type 2 immunity

cellular

abnormal keratinocyte differentiation ( J:226194 )

• marker analysis indicates impaired keratinocyte differentiation

adipose tissue

abnormal hypodermis fat layer morphology ( J:226194 )

• loss of hypodermal fat

Genotype
MGI:5567830

cn41

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Hprt1^{tm1(Ins2-HBEGF)Herr}/Y; Tg(Gcg-rtTA)#Herr/0; Tg(tetO-cre)1Jaw/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6

endocrine/exocrine glands

abnormal pancreatic alpha cell differentiation ( J:159291 )

♂ • alpha cells in diphtheria-treated mice transdifferentiate into beta cells

cellular

abnormal pancreatic alpha cell differentiation ( J:159291 )

♂ • alpha cells in diphtheria-treated mice transdifferentiate into beta cells

Genotype
MGI:6723729

cn42

• Allelic Composition: Amotl1^tm1Laho/Amotl1^tm1Laho; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Tg(Cdh5-cre/ERT2)1Rha/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6

cardiovascular system

abnormal retina vasculature morphology ( J:253854 )

• pups injected with tamoxifen at P1-P3 show a decreased density of the vessel network covering a smaller area of the retina at P6; the vascular density and number of branching points are significantly lower in the periphery and center of P6 retinas

• however, mice injected with tamoxifen at an adult stage show no alterations in the number of branching points and vascular density in adult retinas

abnormal retina blood vessel morphology ( J:253854 )

• pups injected with tamoxifen at P1-P3 show a small but significant reduction in the number of tip cells per vessel length and abnormal pericyte morphology resulting in decreased pericyte coverage of blood vessels in P6 retinas

• however, the number of filopodia per tip cell is relatively normal at P6

abnormal pericyte morphology ( J:253854 )

• pups injected with tamoxifen at P1-P3 show abnormal pericyte morphology, with mural cells "bulging out" from blood vessels, in P6 retinas

vision/eye

abnormal retina vasculature morphology ( J:253854 )

• pups injected with tamoxifen at P1-P3 show a decreased density of the vessel network covering a smaller area of the retina at P6; the vascular density and number of branching points are significantly lower in the periphery and center of P6 retinas

• however, mice injected with tamoxifen at an adult stage show no alterations in the number of branching points and vascular density in adult retinas

abnormal retina blood vessel morphology ( J:253854 )

• pups injected with tamoxifen at P1-P3 show a small but significant reduction in the number of tip cells per vessel length and abnormal pericyte morphology resulting in decreased pericyte coverage of blood vessels in P6 retinas

• however, the number of filopodia per tip cell is relatively normal at P6

Genotype
MGI:5548193

cn43

• Allelic Composition: Ctdnep1^tm3Ryn/Ctdnep1^tm3Ryn; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Six2^{tm1(tTA,tetO-EGFP/cre)Amc}/Six2⁺
• Genetic Background: involves: 129X1/SvJ * C57BL/6 * C57BL/6J

renal/urinary system

decreased kidney apoptosis ( J:205755 )

• apoptotic cells in the nephron as early as P7

cellular

decreased kidney apoptosis ( J:205755 )

• apoptotic cells in the nephron as early as P7

Genotype
MGI:5567828

cn44

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Hprt1^{tm1(Ins2-HBEGF)Herr}/Y; Tg(Ins2-cre/ERT)1Dam/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6 * CBA

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:159291 )

♂N • spared beta cells in diphtheria- and tamoxifen-treated mice do not exhibit increased replication

abnormal pancreatic islet morphology ( J:159291 )

♂ • bihormonal (glucagon+ and insulin+) cells arise in the islets of diphtheria-treated mice

Genotype
MGI:5564909

cn45

• Allelic Composition: Bcl11a^tm1Pwt/Bcl11a^tm1Pwt; Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Tg(Mx1-cre)1Cgn/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6 * CBA

cellular

abnormal dendritic cell differentiation ( J:207383 )

• following pIpC induction cultured precursor cells fail to produce plasmacytoid dendritic cells

hematopoietic system

abnormal dendritic cell differentiation ( J:207383 )

• following pIpC induction cultured precursor cells fail to produce plasmacytoid dendritic cells

decreased dendritic cell number ( J:207383 )

• mild decrease in the total number of cells in GM-CSF-supplemented cultures following pIpC treatment

decreased plasmacytoid dendritic cell number ( J:207383 )

• following pIpC induction cultured precursor cells fail to produce plasmacytoid dendritic cells and in vivo

decreased B cell number ( J:207383 )

• in Flt3L-supplemented cultures following pIpC induced deletion in hematopoietic stem cells and in vivo

immune system

abnormal dendritic cell differentiation ( J:207383 )

• following pIpC induction cultured precursor cells fail to produce plasmacytoid dendritic cells

decreased dendritic cell number ( J:207383 )

• mild decrease in the total number of cells in GM-CSF-supplemented cultures following pIpC treatment

decreased plasmacytoid dendritic cell number ( J:207383 )

• following pIpC induction cultured precursor cells fail to produce plasmacytoid dendritic cells and in vivo

decreased B cell number ( J:207383 )

• in Flt3L-supplemented cultures following pIpC induced deletion in hematopoietic stem cells and in vivo

Genotype
MGI:3831109

cn46

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/?; Tg(Il17f-cre)1Awai/?
• Genetic Background: involves: 129X1/SvJ * C57BL/6 * DBA

normal phenotype

no abnormal phenotype detected ( J:144336 )

Genotype
MGI:4437914

cn47

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Plcg1^tm1Gcrp/Plcg1^tm1Rwen; Tg(Cd4-cre)1Cwi/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6 * DBA/2

immune system

increased T cell apoptosis ( J:157757 )

• following reactivation

abnormal CD4-positive T cell differentiation ( J:157757 )

• differentiation into CD4 or CD8 single positive thymocytes is reduced compared to in wild-type mice

abnormal CD8-positive, alpha-beta T cell differentiation ( J:157757 )

• differentiation into CD4 or CD8 single positive thymocytes is reduced compared to in wild-type mice

increased double-positive T cell number ( J:157757 )

decreased T cell number ( J:157757 )

• peripheral T cells are reduced compared to in wild-type mice

• in transplantation experiments, T cells are less competitive than wild-type T cells

decreased CD4-positive, alpha-beta T cell number ( J:157757 )

• in the thymus

decreased CD8-positive, alpha-beta T cell number ( J:157757 )

• in the thymus

decreased single-positive T cell number ( J:157757 )

• CD4+ thymocytes are more profoundly decreased than CD8+ thymocytes

abnormal T cell activation ( J:157757 )

• mice exhibit an increase in T cell activation compared with wild-type mice

• however, activation phenotype is not cell intrinsic

decreased T cell proliferation ( J:157757 )

• in response to stimulation with anti-CD3m anti-CD3/anti-CD28, or anti-CD3/IL2, T cell proliferation is reduced compared to in similarly treated Plcg1^tm1Gcrp/Plcg1⁺ Tg(CD4-cre)1Cwi Gt(ROSA)26Sor^tm1(EYFP)Cos mice

• however, treatment with PMA/ionomycin restores proliferation

abnormal regulatory T cell physiology ( J:157757 )

• YFP+ T regulatory cells exhibit reduced ability to suppress naive T cell proliferation compared with wild-type T cells

decreased interferon-gamma secretion ( J:157757 )

• following anti-CD3/anti-CD28 stimulation, slightly fewer IFN-gamma producing single positive T cells are detected compared to in similarly treated Plcg1^tm1Gcrp/Plcg1⁺ Tg(CD4-cre)1Cwi Gt(ROSA)26Sor^tm1(EYFP)Cos mice

decreased interleukin-2 secretion ( J:157757 )

• following anti-CD3/anti-CD28 stimulation, IL2 production by single positive T cells is reduced compared to in similarly treated Plcg1^tm1Gcrp/Plcg1⁺ Tg(CD4-cre)1Cwi Gt(ROSA)26Sor^tm1(EYFP)Cos mice

dermatitis ( J:157757 )

• mice exhibit dermatitis unlike wild-type mice

• however, treatment with wild-type T regulatory cells prevents development of symptom

growth/size/body

decreased body weight ( J:157757 )

• mice weight less than wild-type mice

• however, transfer of regulatory T cells restores normal weight gain

digestive/alimentary system

rectal prolapse ( J:157757 )

• mice exhibit rectal prolapse unlike wild-type mice

• however, treatment with wild-type T regulatory cells prevents development of symptom

hematopoietic system

increased T cell apoptosis ( J:157757 )

• following reactivation

abnormal CD4-positive T cell differentiation ( J:157757 )

• differentiation into CD4 or CD8 single positive thymocytes is reduced compared to in wild-type mice

abnormal CD8-positive, alpha-beta T cell differentiation ( J:157757 )

• differentiation into CD4 or CD8 single positive thymocytes is reduced compared to in wild-type mice

increased double-positive T cell number ( J:157757 )

decreased T cell number ( J:157757 )

• peripheral T cells are reduced compared to in wild-type mice

• in transplantation experiments, T cells are less competitive than wild-type T cells

decreased CD4-positive, alpha-beta T cell number ( J:157757 )

• in the thymus

decreased CD8-positive, alpha-beta T cell number ( J:157757 )

• in the thymus

decreased single-positive T cell number ( J:157757 )

• CD4+ thymocytes are more profoundly decreased than CD8+ thymocytes

abnormal T cell activation ( J:157757 )

• mice exhibit an increase in T cell activation compared with wild-type mice

• however, activation phenotype is not cell intrinsic

decreased T cell proliferation ( J:157757 )

• in response to stimulation with anti-CD3m anti-CD3/anti-CD28, or anti-CD3/IL2, T cell proliferation is reduced compared to in similarly treated Plcg1^tm1Gcrp/Plcg1⁺ Tg(CD4-cre)1Cwi Gt(ROSA)26Sor^tm1(EYFP)Cos mice

• however, treatment with PMA/ionomycin restores proliferation

abnormal regulatory T cell physiology ( J:157757 )

• YFP+ T regulatory cells exhibit reduced ability to suppress naive T cell proliferation compared with wild-type T cells

integument

dermatitis ( J:157757 )

• mice exhibit dermatitis unlike wild-type mice

• however, treatment with wild-type T regulatory cells prevents development of symptom

alopecia ( J:157757 )

• mice exhibit alopecia unlike wild-type mice

• however, treatment with wild-type T regulatory cells prevents development of symptom

cellular

increased T cell apoptosis ( J:157757 )

• following reactivation

decreased T cell proliferation ( J:157757 )

• however, treatment with PMA/ionomycin restores proliferation

• in response to stimulation with anti-CD3m anti-CD3/anti-CD28, or anti-CD3/IL2, T cell proliferation is reduced compared to in similarly treated Plcg1^tm1Gcrp/Plcg1⁺ Tg(CD4-cre)1Cwi Gt(ROSA)26Sor^tm1(EYFP)Cos mice

Genotype
MGI:5634193

cn48

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Il22^{tm1.1(icre)Stck}/Il22⁺
• Genetic Background: involves: 129X1/SvJ * C57BL/6N

immune system

abnormal susceptibility to bacterial infection ( J:220074 )

• mice infected with Citrobacter exhibit increased transient weight loss compared with wild-type mice and mice heterozygous for a knock-out allele

• however, mice exhibit normal clearance and kinetics of infection

growth/size/body

increased susceptibility to weight loss ( J:220074 )

• mice infected with Citrobacter exhibit increased transient weight loss compared with wild-type mice and mice heterozygous for a knock-out allele

• however, mice exhibit normal clearance and kinetics of infection

Genotype
MGI:3696478

cn49

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/?; Tg(Lck-cre)548Jxm/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6 * SJL

normal phenotype

no abnormal phenotype detected ( J:117041 )

• mice are viable; strong variation in percentage of RFP-positive T lymphocytes is observed between individual mice, as well as activation in non-T lineage cells

Genotype
MGI:3835668

cn50

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Tg(Plp1-Ncre)DFki/0; Tg(Plp1-Ccre)RFki/0
• Genetic Background: involves: 129X1/SvJ * FVB/N

normal phenotype

no abnormal phenotype detected ( J:144851 )

Genotype
MGI:3835669

cn51

• Allelic Composition: Gt(ROSA)26Sor^tm1(EYFP)Cos/Gt(ROSA)26Sor⁺; Tg(GFAP-Ccre)FFki/0; Tg(GFAP-Ncre)VFki/0
• Genetic Background: involves: 129X1/SvJ * FVB/N

normal phenotype

no abnormal phenotype detected ( J:144851 )