Phenotypes associated with this allele

• Allele Symbol: Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}
• Allele Name: targeted mutation 1, Rudolf Jaenisch
• Allele ID: MGI:3702294
• Summary: 62 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Trim71^tm1695Arte/Trim71^tm1695Arte Tg(tetO-cre)1Jaw/0 Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	B6.Cg-Gt(ROSA)26Sor^tm1(rtTA*M2)Jae Trim71^tm1695Arte Tg(tetO-cre)1Jaw	MGI:7778319
cn2	Rr96^tm1.1Tich/Rr96^+ Gt(ROSA)26Sor^tm1(cre/ERT2)Thl/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae	involves: 129 * 129S4/SvJae * C57BL/6	MGI:5470231
cn3	Acvr1^tm2.1Vlcg/Acvr1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+ Tg(tetO-cre)1Jaw/0	involves: 129 * 129S4/SvJae * C57BL/6 * C57BL/6NTac	MGI:5881968
cn4	Col1a1^tm2(tetO-IDH2*R140Q)Ppp/Col1a1^tm2(tetO-IDH2*R140Q)Ppp Flt3^tm1.1Dosm/Flt3^tm1.1Dosm Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/?	involves: 129 * C57BL/6	MGI:5697542
cn5	Col1a1^tm5(tetO-GFP/RNAi:Cdkn2a)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(Luc)Kael/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae Kras^tm4Tyj/Kras^+ Tg(Scgb1a1-rtTA)1Jaw/0	involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6	MGI:4999988
cn6	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
cn7	Col1a1^tm20(tetO-GFP,-cas9*D10A)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5755882
cn8	Col1a1^tm2(tetO-IDH2*R140Q)Ppp/Col1a1^tm2(tetO-IDH2*R140Q)Ppp Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/?	involves: 129S4/SvJae * C57BL/6	MGI:5697539
cn9	Col1a1^tm17(tetO-GFP,-cas9*)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5755868
cn10	Col1a1^tm18(tetO-GFP,-cas9*)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5755878
cn11	Col1a1^tm19(tetO-GFP,-cas9*)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5755879
cn12	Col1a1^tm1(tetO-EWSR1/ATF1)Yasu/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+ H2az2^Tg(Wnt1-cre)11Rth/H2az2^+ Tg(CAG-cat,-lacZ)11Miya/0	involves: 129S4/SvJae * C57BL/6 * CBA/J * DBA/2	MGI:5485200
cx13	Col1a1^tm9(tetO-GFP/RNAi:Rpa3)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	chimera involves: 129S4/SvJae * C57BL/6	MGI:5000008
cx14	Rr96^tm1.1Tich/Rr96^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129 * 129S4/SvJae * C57BL/6	MGI:5470229
cx15	Rr96^tm1.1Tich/Rr96^tm1.1Tich Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae	involves: 129 * 129S4/SvJae * C57BL/6	MGI:5470230
cx16	Col1a1^tm1(tetO-Irf4)Sing/Col1a1^tm1(tetO-Irf4)Sing Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+ Irf4^tm1Mak/Irf4^+	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6	MGI:5529093
cx17	Col1a1^tm1(tetO-Irf4)Sing/Col1a1^tm1(tetO-Irf4)Sing Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+ Irf4^tm1Mak/Irf4^tm1Mak	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6	MGI:5529094
cx18	Col1a1^tm1(tetO-Yod1*)Hpl/Col1a1^tm1(tetO-Yod1*)Hpl Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae Tap1^tm1Arp/Tap1^tm1Arp	involves: 129S2/SvPas * 129S4/SvJae * C57BL/6	MGI:5478623
cx19	Col1a1^tm11(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae	involves: 129S4/SvJae * C57BL/6	MGI:5000013
cx20	Col1a1^tm1(tetO-Tcfap2c)Hsc/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5051636
cx21	Col1a1^tm1(tetO-RNAi:Rps19)Karl/Col1a1^tm1(tetO-RNAi:Rps19)Karl Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae	involves: 129S4/SvJae * C57BL/6	MGI:5304756
cx22	Col1a1^tm1(tetO-RNAi:Rps19)Karl/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae	involves: 129S4/SvJae * C57BL/6	MGI:5304757
cx23	Col1a1^tm2(tetO-RNAi:Rps19)Karl/Col1a1^tm2(tetO-RNAi:Rps19)Karl Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae	involves: 129S4/SvJae * C57BL/6	MGI:5304758
cx24	Col1a1^tm2(tetO-RNAi:Rps19)Karl/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae	involves: 129S4/SvJae * C57BL/6	MGI:5304759
cx25	Col1a1^tm1(tetO-YAP1*)Fcam/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5316663
cx26	Col1a1^tm1(tetO-Yap1*)Lrsn/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5430595
cx27	Col1a1^tm3(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae/Col1a1^tm3(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae	involves: 129S4/SvJae * C57BL/6	MGI:4430610
cx28	Col1a1^tm6(tetO-MSI2)Jae/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:4822382
cx29	Col1a1^tm1(tetO-GFP/RNAi:luc)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:4999980
cx30	Col1a1^tm3(tetO-GFP/RNAi:Apc)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:4999985
cx31	Col1a1^tm4(tetO-GFP/RNAi:Apc)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:4999987
cx32	Col1a1^tm8(tetO-GFP/RNAi:Rpa3)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae	involves: 129S4/SvJae * C57BL/6	MGI:5000007
cx33	Col1a1^tm10(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5000010
cx34	Col1a1^tm10(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae	involves: 129S4/SvJae * C57BL/6	MGI:5000011
cx35	Col1a1^tm11(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5000012
cx36	Col1a1^tm1(tetO-Yod1*)Hpl/Col1a1^tm1(tetO-Yod1*)Hpl Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae	involves: 129S4/SvJae * C57BL/6	MGI:5478622
cx37	Col1a1^tm1(tetO-EWSR1/ATF1)Yasu/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5485198
cx38	Col1a1^tm3(tetO-Mirlet7g/Mir21)Gqda/? Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5500065
cx39	Col1a1^tm1(tetO-Cyp26b1)Mfra/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5585616
cx40	Col1a1^tm3(tetO-Fosl1,-DsRed)Wag/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5586502
cx41	Col1a1^tm1(tetO-U2AF1*S34F)Mjwa/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/?	involves: 129S4/SvJae * C57BL/6	MGI:5754807
cx42	Col1a1^tm2(tetO-U2AF1)Mjwa/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/0	involves: 129S4/SvJae * C57BL/6	MGI:5754809
cx43	Col1a1^tm2(tetO-Pou5f1)Jae/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:3703249
cx44	Col1a1^tm1(tetO-GFP/RNAi:Rad21)Iaai/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5911575
cx45	Col1a1^tm2(tetO-GFP/RNAi:Smc1a)Iaai/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5911576
cx46	Col1a1^tm3(tetO-GFP/RNAi:Stag2)Iaai/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5911578
cx47	Col1a1^tm2(tetO-GFP/RNAi:Smc1a)Iaai/Col1a1^tm3(tetO-GFP/RNAi:Stag2)Iaai Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6	MGI:5911579
cx48	Col1a1^tm2(tetO-CTNNB1*)Hoch/Col1a1^tm2(tetO-CTNNB1*)Hoch Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/?	involves: 129S4/SvJae * C57BL/6	MGI:5474007
cx49	Apc^Min/Apc^+ Col1a1^tm12(tetO-Dnmt3a_i1)Jae/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:5313423
cx50	Col1a1^tm1(tetO-Deptor)Dmsa/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/?	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:5437856
cx51	Apc^Min/Apc^+ Col1a1^tm9(tetO-Dnmt3b_i1)Jae/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:5313419
cx52	Apc^Min/Apc^+ Col1a1^tm11(tetO-Dnmt3b_i6)Jae/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:5313421
cx53	Apc^Min/Apc^+ Col1a1^tm10(tetO-Dnmt3b_i3)Jae/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:5313420
cx54	Col1a1^tm1(tetO-CTNNB1)Tcd/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:5469373
cx55	Btnl1^tm1(KOMP)Mbp/Btnl1^tm1(KOMP)Mbp Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/0 Tg(tetO-Btnl1)#Ahay/0	involves: 129S4/SvJae * C57BL/6 * C57BL/6N	MGI:6446222
cx56	Col1a1^tm2(tetO-LIN28B)Gqda/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6 * CD-1	MGI:5294614
cx57	Col1a1^tm3(tetO-Mirlet7g/Mir21)Gqda/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6 * CD-1	MGI:5294615
cx58	Col1a1^tm2(tetO-LIN28B)Gqda/Col1a1^tm3(tetO-Mirlet7g/Mir21)Gqda Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6 * CD-1	MGI:5294616
cx59	Col1a1^tm10(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+ Tg(CMV-rtTA)4Bjd/0	involves: 129S4/SvJae * C57BL/6 * NMRI	MGI:5000009
cx60	Col1a1^tm8(tetO-GFP/RNAi:Rpa3)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+ Tg(CMV-rtTA)4Bjd/0	involves: 129S4/SvJae * C57BL/6 * NMRI	MGI:5000006
cx61	Col1a1^tm11(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+ Tg(CMV-rtTA)4Bjd/0	involves: 129S4/SvJae * C57BL/6 * NMRI	MGI:5000014
cx62	Col1a1^tm1(tetO-Stat1)Biat/Col1a1^tm1(tetO-Stat1)Biat Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^tm1(rtTA*M2)Jae Stat1^tm1Dlv/Stat1^tm1Dlv	involves: 129S/SvEv * 129S4/SvJae * C57BL/6	MGI:5698051

Genotype
MGI:7778319

cn1

• Allelic Composition: Trim71^tm1695Arte/Trim71^tm1695Arte; Tg(tetO-cre)1Jaw/0; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: B6.Cg-Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae} Trim71^tm1695Arte Tg(tetO-cre)1Jaw

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

embryo

abnormal neural tube morphology ( J:335575 )

• doxycycline treatment at E5.5 results in completely penetrant neural tube defects at E12.5

• however, doxycycline treatment at P0.5 results in normal brain development

nervous system

abnormal neural tube morphology ( J:335575 )

• doxycycline treatment at E5.5 results in completely penetrant neural tube defects at E12.5

• however, doxycycline treatment at P0.5 results in normal brain development

Genotype
MGI:5470231

cn2

• Allelic Composition: Rr96^tm1.1Tich/Rr96⁺; Gt(ROSA)26Sor^{tm1(cre/ERT2)Thl}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}
• Genetic Background: involves: 129 * 129S4/SvJae * C57BL/6

immune system

abnormal T cell differentiation ( J:191711 )

• derepression of Cd4 occurs in all CD4^- T cells

• T cell expression of CD4 increases rapidly after cre activation

hematopoietic system

abnormal T cell differentiation ( J:191711 )

• derepression of Cd4 occurs in all CD4^- T cells

• T cell expression of CD4 increases rapidly after cre activation

Genotype
MGI:5881968

cn3

• Allelic Composition: Acvr1^tm2.1Vlcg/Acvr1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺; Tg(tetO-cre)1Jaw/0
• Genetic Background: involves: 129 * 129S4/SvJae * C57BL/6 * C57BL/6NTac

skeleton

increased bone ossification ( J:239136 )

• mice treated with doxycycline at 1 month of age for 3 days then injected with cardiotoxin into the quadriceps muscle to induce inflammation and muscle damage develop large heterotopic ossification tissue masses

• treatment of cardiotoxin-induced muscle injury with palovarotene diminishes heterotopic ossification formation by more than 80%

behavior/neurological

abnormal motor capabilities/coordination/movement ( J:239136 )

• about 14 days after heterotopic ossification induction by injury in doxycycline treated mice, movement of affected legs is impaired

• treatment with palovarotene of mice with cardiotoxin-induced muscle injury rescues the impaired movement

Genotype
MGI:5697542

cn4

• Allelic Composition: Col1a1^{tm2(tetO-IDH2*R140Q)Ppp}/Col1a1^{tm2(tetO-IDH2*R140Q)Ppp}; Flt3^tm1.1Dosm/Flt3^tm1.1Dosm; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/?
• Genetic Background: involves: 129 * C57BL/6

neoplasm

increased leukemia incidence ( J:210097 )

• mice treated with doxycycline develop acute leukemias

mortality/aging

premature death ( J:210097 )

• reduced overall survival of doxycycline treated mice to 229 days vs 352 days for Flt3^tm1.1Dosm controls

Genotype
MGI:4999988

cn5

• Allelic Composition: Col1a1^{tm5(tetO-GFP/RNAi:Cdkn2a)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^tm1(Luc)Kael/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}; Kras^tm4Tyj/Kras⁺; Tg(Scgb1a1-rtTA)1Jaw/0
• Genetic Background: involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6

mortality/aging

premature death ( J:171191 )

• mice treated with a cre-expressing adenovirus and treated with doxycycline exhibit reduced survival compared with control mice

neoplasm

increased tumor incidence ( J:171191 )

• mice treated with a cre-expressing adenovirus and treated with doxycycline exhibit increased tumor incidence (size and number) in the lungs with rare noninvasive lung adenomas compared with control mice

• however, mice treated with a cre-expressing adenovirus and treated with doxycycline exhibit tumor regression after doxycycline removal

increased lung adenoma incidence ( J:171191 )

• in mice treated with a cre-expressing adenovirus and treated with doxycycline

respiratory system

increased lung adenoma incidence ( J:171191 )

• in mice treated with a cre-expressing adenovirus and treated with doxycycline

respiratory distress ( J:171191 )

• rapid shallow breathing in mice treated with a cre-expressing adenovirus and treated with doxycycline

growth/size/body

cachexia ( J:171191 )

• in mice treated with a cre-expressing adenovirus and treated with doxycycline

Genotype
MGI:5485201

cn6

• 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:5755882

cn7

• Allelic Composition: Col1a1^{tm20(tetO-GFP,-cas9*D10A)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

digestive/alimentary system

ectopic Paneth cells ( J:222595 )

• increased in doxycycline-treated mice

abnormal small intestinal crypt cell physiology ( J:222595 )

• doxycycline-treated mice exhibit dramatic hyper-proliferation and crypt expansion, blocked differentiation and ectopic Paneth cell production compared with control mice

abnormal small intestinal crypt cell proliferation ( J:222595 )

• increased in doxycycline-treated mice

cellular

abnormal small intestinal crypt cell proliferation ( J:222595 )

• increased in doxycycline-treated mice

endocrine/exocrine glands

ectopic Paneth cells ( J:222595 )

• increased in doxycycline-treated mice

Genotype
MGI:5697539

cn8

• Allelic Composition: Col1a1^{tm2(tetO-IDH2*R140Q)Ppp}/Col1a1^{tm2(tetO-IDH2*R140Q)Ppp}; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/?
• Genetic Background: involves: 129S4/SvJae * C57BL/6

hematopoietic system

hematopoietic system phenotype ( J:210097 )

N • modified IDH2 expression induced by doxycycline in chow starting around 3 weeks

N • peripheral blood cell counts, number of hematopoietic stem cells, myeloid progenitors, mature B and T lymphocytes, and myeloid cells all normal when examined 8 weeks after induction

abnormal hematopoietic stem cell proliferation ( J:210097 )

• KSL cells collected and plated out 8 weeks after induction display severely reduced erythroid colony formation but myeloid colony numbers are normal

• differentiation blockade is removed when doxycycline is removed from the culture medium

increased hematopoietic stem cell proliferation ( J:210097 )

• by 7 months KSL cells are increased in bone marrow relative to controls

• long-term hematopoietic stem cells also tend to expand in number

enlarged spleen ( J:210097 )

• about 1.3X larger than control spleens

extramedullary hematopoiesis ( J:210097 )

• significant extramedullary hematopoiesis

neoplasm

neoplasm ( J:210097 )

N • no mice on doxycycline treatment for 1 year develop leukemia

increased leukemia incidence ( J:210097 )

• infection of KSL cells with retrovirus containing HoxA9 and Meis1 and then injected into sub-lethally irradiated mice results in a pre-leukemic cell expansion

cellular

abnormal hematopoietic stem cell proliferation ( J:210097 )

• KSL cells collected and plated out 8 weeks after induction display severely reduced erythroid colony formation but myeloid colony numbers are normal

• differentiation blockade is removed when doxycycline is removed from the culture medium

increased hematopoietic stem cell proliferation ( J:210097 )

• by 7 months KSL cells are increased in bone marrow relative to controls

• long-term hematopoietic stem cells also tend to expand in number

immune system

enlarged spleen ( J:210097 )

• about 1.3X larger than control spleens

growth/size/body

enlarged spleen ( J:210097 )

• about 1.3X larger than control spleens

Genotype
MGI:5755868

cn9

• Allelic Composition: Col1a1^{tm17(tetO-GFP,-cas9*)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

digestive/alimentary system

ectopic Paneth cells ( J:222595 )

• increased in doxycycline-treated mice

abnormal small intestinal crypt cell physiology ( J:222595 )

• doxycycline-treated mice exhibit dramatic hyper-proliferation and crypt expansion, blocked differentiation and ectopic Paneth cell production compared with control mice

abnormal small intestinal crypt cell proliferation ( J:222595 )

• increased in doxycycline-treated mice

endocrine/exocrine glands

ectopic Paneth cells ( J:222595 )

• increased in doxycycline-treated mice

cellular

abnormal small intestinal crypt cell proliferation ( J:222595 )

• increased in doxycycline-treated mice

Genotype
MGI:5755878

cn10

• Allelic Composition: Col1a1^{tm18(tetO-GFP,-cas9*)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

digestive/alimentary system

digestive/alimentary phenotype ( J:222595 )

N • doxycycline-treated mice exhibit normal crypt proliferation, differentiation and Paneth cell production

Genotype
MGI:5755879

cn11

• Allelic Composition: Col1a1^{tm19(tetO-GFP,-cas9*)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

digestive/alimentary system

ectopic Paneth cells ( J:222595 )

• increased in doxycycline-treated mice

abnormal small intestinal crypt cell physiology ( J:222595 )

• doxycycline-treated mice exhibit dramatic hyper-proliferation and crypt expansion, blocked differentiation and ectopic Paneth cell production compared with control mice

abnormal small intestinal crypt cell proliferation ( J:222595 )

• increased in doxycycline-treated mice

cellular

abnormal small intestinal crypt cell proliferation ( J:222595 )

• increased in doxycycline-treated mice

endocrine/exocrine glands

ectopic Paneth cells ( J:222595 )

• increased in doxycycline-treated mice

Genotype
MGI:5485200

cn12

• Allelic Composition: Col1a1^{tm1(tetO-EWSR1/ATF1)Yasu}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺; H2az2^{Tg(Wnt1-cre)11Rth}/H2az2⁺; Tg(CAG-cat,-lacZ)11Miya/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * CBA/J * DBA/2

neoplasm

increased sarcoma incidence ( J:194505 )

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

Genotype
MGI:5000008

cx13

• Allelic Composition: Col1a1^{tm9(tetO-GFP/RNAi:Rpa3)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: chimera involves: 129S4/SvJae * C57BL/6

reproductive system

infertility ( J:171348 )

• the founder mouse is sterile

Genotype
MGI:5470229

cx14

• Allelic Composition: Rr96^tm1.1Tich/Rr96⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129 * 129S4/SvJae * C57BL/6

immune system

abnormal CD4-positive T cell differentiation ( J:191711 )

• 15 days of doxycycline exposure leads to CD4 induction in all but the earliest CD4^- thymocytes (not in DN1-3)

• only about 30% of peripheral CD8 cells begin expressing CD4

hematopoietic system

abnormal CD4-positive T cell differentiation ( J:191711 )

• 15 days of doxycycline exposure leads to CD4 induction in all but the earliest CD4^- thymocytes (not in DN1-3)

• only about 30% of peripheral CD8 cells begin expressing CD4

Genotype
MGI:5470230

cx15

• Allelic Composition: Rr96^tm1.1Tich/Rr96^tm1.1Tich; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}
• Genetic Background: involves: 129 * 129S4/SvJae * C57BL/6

immune system

abnormal T cell differentiation ( J:191711 )

• doxycycline treatment leads to detectable CD4⁺ CD8⁺ cells after 2 days

• levels of double positive cells reach 47% by 17 days after the start of treatment

hematopoietic system

abnormal T cell differentiation ( J:191711 )

• doxycycline treatment leads to detectable CD4⁺ CD8⁺ cells after 2 days

• levels of double positive cells reach 47% by 17 days after the start of treatment

Genotype
MGI:5529093

cx16

• Allelic Composition: Col1a1^{tm1(tetO-Irf4)Sing}/Col1a1^{tm1(tetO-Irf4)Sing}; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺; Irf4^tm1Mak/Irf4⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6

hematopoietic system

abnormal class switch recombination ( J:203903 )

• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination

abnormal plasma cell differentiation ( J:203903 )

• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination

immune system

abnormal class switch recombination ( J:203903 )

• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination

abnormal plasma cell differentiation ( J:203903 )

• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination

Genotype
MGI:5529094

cx17

• Allelic Composition: Col1a1^{tm1(tetO-Irf4)Sing}/Col1a1^{tm1(tetO-Irf4)Sing}; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺; Irf4^tm1Mak/Irf4^tm1Mak
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6

hematopoietic system

abnormal class switch recombination ( J:203903 )

• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination but not as severe as in mice heterozygous for Irf4^tm1Mak

abnormal plasma cell differentiation ( J:203903 )

• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination but not as severe as in mice heterozygous for Irf4^tm1Mak

immune system

abnormal class switch recombination ( J:203903 )

• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination but not as severe as in mice heterozygous for Irf4^tm1Mak

abnormal plasma cell differentiation ( J:203903 )

• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination but not as severe as in mice heterozygous for Irf4^tm1Mak

Genotype
MGI:5478623

cx18

• Allelic Composition: Col1a1^{tm1(tetO-Yod1*)Hpl}/Col1a1^{tm1(tetO-Yod1*)Hpl}; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}; Tap1^tm1Arp/Tap1^tm1Arp
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * C57BL/6

immune system

abnormal professional antigen presenting cell physiology ( J:194608 )

• APCs from doxycycline-treated mice exhibit enhanced antigen cross-presentation compared with control cells

Genotype
MGI:5000013

cx19

• Allelic Composition: Col1a1^{tm11(tetO*-RFP/RNAi:Rpa3)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:171348 )

• all mice treated with doxycycline between 5 and 10 weeks of age die prematurely

digestive/alimentary system

abnormal small intestinal crypt cell physiology ( J:171348 )

• doxycycline-treated adult mice exhibit atrophy of intestinal epithelium unlike control mice

• however, withdrawal of doxycycline reverses villus atrophy

abnormal small intestinal crypt cell proliferation ( J:171348 )

• doxycycline-treated adult mice exhibit decreased proliferation and cell cycle arrest in the intestinal epithelium unlike control mice

hematopoietic system

decreased erythroid progenitor cell number ( J:171348 )

• doxycycline-treated adult mice exhibit decreased erythroid precursors in the bone marrow unlike in control mice

growth/size/body

weight loss ( J:171348 )

• in doxycycline-treated adult mice

• however, mice regain weight after withdrawal of doxycycline

cellular

abnormal small intestinal crypt cell proliferation ( J:171348 )

• doxycycline-treated adult mice exhibit decreased proliferation and cell cycle arrest in the intestinal epithelium unlike control mice

Genotype
MGI:5051636

cx20

• Allelic Composition: Col1a1^{tm1(tetO-Tcfap2c)Hsc}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

Col1a1^{tm1(tetO-Tcfap2c)Hsc}/Col1a1⁺ Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺ mice show increased proliferation and induced hepatic steatosis

mortality/aging

premature death ( J:174049 )

• within 6 to 7 days of doxycycline treatment

homeostasis/metabolism

abnormal circulating enzyme level ( J:174049 )

• after doxycycline treatment, mice exhibit increased serum levels of aspartate transaminase, alanine transaminase, alkaline phosphatase, lipase, amylase, lactate dehydrogenase levels compared with control mice

increased circulating alanine transaminase level ( J:174049 )

• after doxycycline treatment

increased circulating alkaline phosphatase level ( J:174049 )

• after doxycycline treatment

increased circulating amylase level ( J:174049 )

• after doxycycline treatment

increased circulating aspartate transaminase level ( J:174049 )

• after doxycycline treatment

increased circulating lactate dehydrogenase level ( J:174049 )

• after doxycycline treatment

dehydration ( J:174049 )

• after doxycycline treatment

decreased liver glycogen level ( J:174049 )

• after doxycycline treatment

liver/biliary system

increased hepatocyte apoptosis ( J:174049 )

• after doxycycline treatment

increased hepatocyte proliferation ( J:174049 )

• after doxycycline treatment

decreased liver glycogen level ( J:174049 )

• after doxycycline treatment

abnormal hepatocyte morphology ( J:174049 )

• after doxycycline treatment, hepatocytes exhibit abnormally bright mitochondria and increased mitophagy compared to in cells from control mice

abnormal hepatocyte mitochondrial morphology ( J:174049 )

• after doxycycline treatment, hepatocytes exhibit abnormally bright mitochondria

microvesicular hepatic steatosis ( J:174049 )

• after doxycycline treatment, mice exhibit microvesicular steatosis unlike control mice

liver failure ( J:174049 )

• after doxycycline treatment

digestive/alimentary system

abnormal enterocyte proliferation ( J:174049 )

• after doxycycline treatment, the proliferative zone is expanded to cover crypt and villus compared to in control mice

abnormal intestine development ( J:174049 )

• after doxycycline treatment, the number of terminally differentiated intestinal cells (absorptive enterocytes, goblet cells, Paneth, cells and enteroendocrine cells) is reduced compared to in control mice

abnormal intestinal mucosa morphology ( J:174049 )

• after doxycycline treatment

abnormal small intestine morphology ( J:174049 )

• after doxycycline treatment, the ratio of crypt length to villus length in the duodenum, jejunum, and ileum is increased compared to in control mice

endocrine/exocrine glands

abnormal pancreas physiology ( J:174049 )

• after doxycycline treatment, mice exhibit pancreatic injury unlike control mice

behavior/neurological

lethargy ( J:174049 )

• after doxycycline treatment

growth/size/body

weight loss ( J:174049 )

• after doxycycline treatment

immune system

immune system phenotype ( J:174049 )

N • doxycycline-treated mice do not exhibit induction of inflammatory processes

cellular

abnormal hepatocyte mitochondrial morphology ( J:174049 )

• after doxycycline treatment, hepatocytes exhibit abnormally bright mitochondria

increased hepatocyte apoptosis ( J:174049 )

• after doxycycline treatment

abnormal enterocyte proliferation ( J:174049 )

• after doxycycline treatment, the proliferative zone is expanded to cover crypt and villus compared to in control mice

increased hepatocyte proliferation ( J:174049 )

• after doxycycline treatment

Genotype
MGI:5304756

cx21

• Allelic Composition: Col1a1^{tm1(tetO-RNAi:Rps19)Karl}/Col1a1^{tm1(tetO-RNAi:Rps19)Karl}; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:179085 )

• most mice die within 2 months following doxycycline treatment

hematopoietic system

abnormal bone marrow cell morphology/development ( J:179085 )

• decrease in the frequency of bipotential megakaryocytic-erythroid cells and preGM/GMP progenitor cells at 7 weeks after doxycycline treatment

decreased bone marrow cell number ( J:179085 )

• by 10 days after doxycycline treatment

• absolute numbers of all hematopoietic stem and progenitor cells are reduced at 7 weeks after doxycycline treatment

decreased megakaryocyte cell number ( J:179085 )

• seven weeks after doxycycline treatment

abnormal proerythroblast morphology ( J:179085 )

• decrease in the frequency or proerythroblasts in the bone marrow by 10 days after doxycycline treatment

macrocytosis ( J:179085 )

• seven weeks after doxycycline treatment

thrombocytosis ( J:179085 )

• two weeks after doxycycline treatment

decreased hematopoietic cell number ( J:179085 )

decreased erythrocyte cell number ( J:179085 )

• two and seven weeks after doxycycline treatment

decreased neutrophil cell number ( J:179085 )

• seven weeks after doxycycline treatment

thrombocytopenia ( J:179085 )

• seven weeks after doxycycline treatment

decreased lymphocyte cell number ( J:179085 )

• two and seven weeks after doxycycline treatment

reticulocytopenia ( J:179085 )

• two weeks after doxycycline treatment

abnormal bone marrow cell physiology ( J:179085 )

• preMegE and preCFU-E/CFU-E progenitors show impaired proliferation and increased apoptosis following doxycycline treatment

growth/size/body

postnatal growth retardation ( J:179085 )

• following doxycycline treatment

digestive/alimentary system

abnormal large intestine morphology ( J:179085 )

• occasional dilated glands in the large intestine and colon

immune system

decreased neutrophil cell number ( J:179085 )

• seven weeks after doxycycline treatment

decreased lymphocyte cell number ( J:179085 )

• two and seven weeks after doxycycline treatment

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Diamond-Blackfan anemia		DOID:1339	OMIM:PS105650	J:179085

Genotype
MGI:5304757

cx22

• Allelic Composition: Col1a1^{tm1(tetO-RNAi:Rps19)Karl}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

mortality/aging ( J:179085 )

N • unlike homozygous mice, heterozygotes survive at least 3 months following doxycycline treatment

hematopoietic system

abnormal bone marrow cell morphology/development ( J:179085 )

• decrease in the frequency of bipotential megakaryocytic-erythroid cells and preGM/GMP progenitor cells at 7 weeks after doxycycline treatment

decreased bone marrow cell number ( J:179085 )

• by 10 days after doxycycline treatment

• absolute numbers of all hematopoietic stem and progenitor cells are reduced at 7 weeks after doxycycline treatment

decreased megakaryocyte cell number ( J:179085 )

• seven weeks after doxycycline treatment

abnormal proerythroblast morphology ( J:179085 )

• decrease in the frequency or proerythroblasts in the bone marrow by 10 days after doxycycline treatment

macrocytosis ( J:179085 )

• seven weeks after doxycycline treatment

thrombocytosis ( J:179085 )

• two weeks after doxycycline treatment

decreased hematopoietic cell number ( J:179085 )

decreased erythrocyte cell number ( J:179085 )

• two and seven weeks after doxycycline treatment

decreased lymphocyte cell number ( J:179085 )

• two and seven weeks after doxycycline treatment

reticulocytopenia ( J:179085 )

• two weeks after doxycycline treatment

abnormal bone marrow cell physiology ( J:179085 )

• preMegE and preCFU-E/CFU-E progenitors show impaired proliferation and increased apoptosis following doxycycline treatment

immune system

decreased lymphocyte cell number ( J:179085 )

• two and seven weeks after doxycycline treatment

growth/size/body

postnatal growth retardation ( J:179085 )

• less pronounced than in homozygous mice

• following doxycycline treatment

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Diamond-Blackfan anemia		DOID:1339	OMIM:PS105650	J:179085

Genotype
MGI:5304758

cx23

• Allelic Composition: Col1a1^{tm2(tetO-RNAi:Rps19)Karl}/Col1a1^{tm2(tetO-RNAi:Rps19)Karl}; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:179085 )

• most mice die within 2 months following doxycycline treatment

hematopoietic system

macrocytosis ( J:179085 )

• seven weeks after doxycycline treatment

thrombocytosis ( J:179085 )

• two weeks after doxycycline treatment

decreased hematopoietic cell number ( J:179085 )

decreased erythrocyte cell number ( J:179085 )

• two and seven weeks after doxycycline treatment

decreased neutrophil cell number ( J:179085 )

• seven weeks after doxycycline treatment

thrombocytopenia ( J:179085 )

• seven weeks after doxycycline treatment

decreased lymphocyte cell number ( J:179085 )

• two and seven weeks after doxycycline treatment

reticulocytopenia ( J:179085 )

• two weeks after doxycycline treatment

growth/size/body

postnatal growth retardation ( J:179085 )

• following doxycycline treatment

immune system

decreased neutrophil cell number ( J:179085 )

• seven weeks after doxycycline treatment

decreased lymphocyte cell number ( J:179085 )

• two and seven weeks after doxycycline treatment

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Diamond-Blackfan anemia		DOID:1339	OMIM:PS105650	J:179085

Genotype
MGI:5304759

cx24

• Allelic Composition: Col1a1^{tm2(tetO-RNAi:Rps19)Karl}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

mortality/aging ( J:179085 )

N • unlike homozygous mice, heterozygotes survive at least 3 months following doxycycline treatment

hematopoietic system

macrocytosis ( J:179085 )

• seven weeks after doxycycline treatment

thrombocytosis ( J:179085 )

• two weeks after doxycycline treatment

decreased hematopoietic cell number ( J:179085 )

decreased erythrocyte cell number ( J:179085 )

• two and seven weeks after doxycycline treatment

thrombocytopenia ( J:179085 )

• seven weeks after doxycycline treatment

decreased lymphocyte cell number ( J:179085 )

• two and seven weeks after doxycycline treatment

reticulocytopenia ( J:179085 )

• two weeks after doxycycline treatment

growth/size/body

postnatal growth retardation ( J:179085 )

• following doxycycline treatment

• less pronounced than in homozygous mice

immune system

decreased lymphocyte cell number ( J:179085 )

• two and seven weeks after doxycycline treatment

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Diamond-Blackfan anemia		DOID:1339	OMIM:PS105650	J:179085

Genotype
MGI:5316663

cx25

• Allelic Composition: Col1a1^{tm1(tetO-YAP1*)Fcam}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:141457 )

• mice become ill and must be euthanized 4-6 days after doxycycline treatment

digestive/alimentary system

abnormal intestinal goblet cell morphology ( J:141457 )

• mature goblet cells are absent 5 days after doxycycline treatment

• however, the absence of mature goblet cells is reversed by doxycycline-withdrawal and administration of dipenzazepine increased goblet cell numbers

abnormal enterocyte proliferation ( J:141457 )

• increased proliferation of epithelium cells in the crypt regions, villus regions and at the tip of the villi of undifferentiated progenitor cells in doxycycline-treated mice

• dipenzazepine administration decreases cell proliferation in the intestine of mice treated with doxycycline

• however, proliferation of undifferentiated cells is reversed by doxycycline-withdrawal

increased pancreatic acinar cell number ( J:141457 )

• in doxycycline-treated mice

abnormal intestinal epithelium morphology ( J:141457 )

• severe dysplasia in doxycycline-treated mice

absent Paneth cells ( J:141457 )

• Paneth cells are absent 5 days after doxycycline treatment

• however, the absence of Paneth cells is reversed by doxycycline-withdrawal

endocrine/exocrine glands

increased pancreatic acinar cell number ( J:141457 )

• in doxycycline-treated mice

absent Paneth cells ( J:141457 )

• Paneth cells are absent 5 days after doxycycline treatment

• however, the absence of Paneth cells is reversed by doxycycline-withdrawal

enlarged pancreas ( J:141457 )

• in doxycycline-treated mice

pancreatic acinar-to-ductal metaplasia ( J:141457 )

• ductal metaplasia of pancreatic acinar cells in doxycycline-treated mice

cellular

abnormal intestinal goblet cell morphology ( J:141457 )

• mature goblet cells are absent 5 days after doxycycline treatment

• however, the absence of mature goblet cells is reversed by doxycycline-withdrawal and administration of dipenzazepine increased goblet cell numbers

abnormal enterocyte proliferation ( J:141457 )

• increased proliferation of epithelium cells in the crypt regions, villus regions and at the tip of the villi of undifferentiated progenitor cells in doxycycline-treated mice

• dipenzazepine administration decreases cell proliferation in the intestine of mice treated with doxycycline

• however, proliferation of undifferentiated cells is reversed by doxycycline-withdrawal

increased cell proliferation ( J:141457 )

• in the epidermis of doxycycline-treated mice

homeostasis/metabolism

decreased alkaline phosphatase activity ( J:141457 )

• absent in the small intestine 5 days after doxycycline treatment

integument

thick skin ( J:141457 )

• in doxycycline-treated mice

growth/size/body

enlarged pancreas ( J:141457 )

• in doxycycline-treated mice

Genotype
MGI:5430595

cx26

• Allelic Composition: Col1a1^{tm1(tetO-Yap1*)Lrsn}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:185310 )

• all mice die 10 days after treatment with doxycycline

Genotype
MGI:4430610

cx27

• Allelic Composition: Col1a1^{tm3(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae}/Col1a1^{tm3(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae}; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}
• Genetic Background: involves: 129S4/SvJae * C57BL/6

normal phenotype

no abnormal phenotype detected ( J:157298 )

• mice exhibit no tumors or health problems up to 31 weeks

Genotype
MGI:4822382

cx28

• Allelic Composition: Col1a1^{tm6(tetO-MSI2)Jae}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:163322 )

• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 die within 14 days due to rapid and lethal myeloproliferative disease

hematopoietic system

enlarged spleen ( J:163322 )

• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 exhibit increased liver size compared with similarly treated mice reconstituted with wild-type bone marrow

increased spleen weight ( J:163322 )

• modestly in doxycycline-treated wild-type mice reconstituted with bone marrow

• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

spleen hyperplasia ( J:163322 )

• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

abnormal myelopoiesis ( J:163322 )

• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 die within 14 days due to rapid and lethal myeloproliferative disease

abnormal bone marrow cell morphology/development ( J:163322 )

decreased common myeloid progenitor cell number ( J:163322 )

• wild-type mice reconstituted with bone marrow and treated with doxycycline exhibit a decrease in myeloid progenitor and myeloid erythrocroid progenitor cells compared with mice reconstituted with wild-type bone marrow

increased bone marrow cell number ( J:163322 )

• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

abnormal erythrocyte morphology ( J:163322 )

increased erythrocyte cell number ( J:163322 )

• at 6 weeks, but not 16 weeks, in wild-type mice reconstituted with bone marrow and treated with doxycyline

increased hematocrit ( J:163322 )

• at 6 and 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline

increased mean corpuscular volume ( J:163322 )

• at 6 and 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline

thrombocytopenia ( J:163322 )

• at 6 weeks, but not 16 weeks, in wild-type mice reconstituted with bone marrow and treated with doxycyline

increased hematopoietic stem cell number ( J:163322 )

• doxycycline-treated mice exhibit an expansion of hematopoietic stem cells (HSCs) due to preferential expansion of short term HSC compared with wild-type mice

• wild-type mice reconstituted with bone marrow and treated with doxycycline exhibit an increase in HSCs, hematopoietic progenitor cells, and long term HSCs compared with mice reconstituted with wild-type bone marrow

abnormal leukocyte morphology ( J:163322 )

decreased neutrophil cell number ( J:163322 )

• at 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline

decreased lymphocyte cell number ( J:163322 )

• at 6 and 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline

increased leukocyte cell number ( J:163322 )

• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

liver/biliary system

increased liver weight ( J:163322 )

• modestly in doxycycline-treated wild-type mice reconstituted with bone marrow

• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

neoplasm

increased leukemia incidence ( J:163322 )

• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 exhibit an increase in the number of leukemic blasts and infiltration with immature myeloid cells compared with similarly treated wild-type mice reconstituted with wild-type bone marrow

immune system

enlarged spleen ( J:163322 )

• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 exhibit increased liver size compared with similarly treated mice reconstituted with wild-type bone marrow

increased spleen weight ( J:163322 )

• modestly in doxycycline-treated wild-type mice reconstituted with bone marrow

• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

spleen hyperplasia ( J:163322 )

• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

abnormal myelopoiesis ( J:163322 )

• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 die within 14 days due to rapid and lethal myeloproliferative disease

abnormal leukocyte morphology ( J:163322 )

decreased neutrophil cell number ( J:163322 )

• at 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline

decreased lymphocyte cell number ( J:163322 )

• at 6 and 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline

increased leukocyte cell number ( J:163322 )

• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

growth/size/body

increased liver weight ( J:163322 )

• modestly in doxycycline-treated wild-type mice reconstituted with bone marrow

• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

enlarged spleen ( J:163322 )

• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 exhibit increased liver size compared with similarly treated mice reconstituted with wild-type bone marrow

increased spleen weight ( J:163322 )

• modestly in doxycycline-treated wild-type mice reconstituted with bone marrow

• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

spleen hyperplasia ( J:163322 )

• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

Genotype
MGI:4999980

cx29

• Allelic Composition: Col1a1^{tm1(tetO-GFP/RNAi:luc)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

normal phenotype

no abnormal phenotype detected ( J:171191 )

• doxycycline-treated mice are normal

Genotype
MGI:4999985

cx30

• Allelic Composition: Col1a1^{tm3(tetO-GFP/RNAi:Apc)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:171191 )

• doxycycline-treated mice with lymphoma exhibit median survival of 7.4 months

skeleton

delayed endochondral bone ossification ( J:171191 )

• at E14.5 and E18.5, mice treated with doxycycline at E8.5 exhibit severely delayed or absent endochondral ossification of multiple skeletal elements (spine, ribs, and limbs) compared with wild-type mice

• mice transiently treated with doxycycline between E8.5 and E12.5 exhibit some reduced bone growth (ribs, spine, and skull) compared with wild-type mice

failure of endochondral bone ossification ( J:171191 )

• at E14.5 and E18.5, mice treated with doxycycline at E8.5 exhibit severely delayed or absent endochondral ossification of multiple skeletal elements (spine, ribs, and limbs) compared with wild-type mice

• mice transiently treated with doxycycline between E8.5 and E12.5 exhibit some reduced bone growth (ribs, spine, and skull) compared with wild-type mice

integument

excessive hair ( J:171191 )

• mice treated with doxycycline for 6 weeks (either initiated at birth or 4 to 6 weeks of age) exhibit excessive hair growth compared with wild-type mice

progressive hair loss ( J:171191 )

• in mice treated with doxycycline beyond 20 weeks

• however, reactivation after 4 weeks by doxycycline withdrawal prevents hair loss

abnormal hair follicle morphology ( J:171191 )

• in mice treated with doxycycline beyond 20 weeks

homeostasis/metabolism

hydrops fetalis ( J:171191 )

• in mice treated with doxycycline at E8.5

• however, mice transiently treated with doxycycline between E8.5 and E12.5 do not exhibit edema

limbs/digits/tail

polydactyly ( J:171191 )

• mice transiently treated with doxycycline between E8.5 and E12.5 exhibit extra digits (total 5 to 9) that are largely unsegmented and duplicated along their length compared with wild-type mice

abnormal forelimb morphology ( J:171191 )

• mice transiently treated with doxycycline between E8.5 and E12.5 exhibit severely stunted hind- and forelimb development compared with wild-type mice

abnormal hindlimb morphology ( J:171191 )

• mice transiently treated with doxycycline between E8.5 and E12.5 exhibit severely stunted hind- and forelimb development compared with wild-type mice

growth/size/body

short snout ( J:171191 )

• in mice treated with doxycycline 1 to 2 days prior to birth

• reactivation after 4 weeks of doxycycline treatment does not rescue stunted snout

decreased body size ( J:171191 )

• runting in mice treated with doxycycline 1 to 2 days prior to birth

postnatal growth retardation ( J:171191 )

• in mice treated with doxycycline 1 to 2 days prior to birth

fetal growth retardation ( J:171191 )

• at E14.5 and E18.5 in mice treated with doxycycline at E8.5

neoplasm

increased leukemia incidence ( J:171191 )

• in mice treated with doxycycline from 4 to 6 weeks of age

increased lymphoma incidence ( J:171191 )

• in the thymus and lymph nodes of mice treated with doxycycline from 4 to 6 weeks of age

increased T cell derived lymphoma incidence ( J:171191 )

• in mice treated with doxycycline from 4 to 6 weeks of age

craniofacial

short snout ( J:171191 )

• in mice treated with doxycycline 1 to 2 days prior to birth

• reactivation after 4 weeks of doxycycline treatment does not rescue stunted snout

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:171191 )

• in mice treated with doxycycline from 4 to 6 weeks of age

immune system

increased T cell derived lymphoma incidence ( J:171191 )

• in mice treated with doxycycline from 4 to 6 weeks of age

hematopoietic system

increased T cell derived lymphoma incidence ( J:171191 )

• in mice treated with doxycycline from 4 to 6 weeks of age

Genotype
MGI:4999987

cx31

• Allelic Composition: Col1a1^{tm4(tetO-GFP/RNAi:Apc)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:171191 )

• doxycycline-treated mice with lymphoma exhibit median survival or 5.3 months

neoplasm

increased leukemia incidence ( J:171191 )

• in mice treated with doxycycline from 4 to 6 weeks of age

increased lymphoma incidence ( J:171191 )

• in the thymus and lymph nodes of mice treated with doxycycline from 4 to 6 weeks of age

increased T cell derived lymphoma incidence ( J:171191 )

• in mice treated with doxycycline from 4 to 6 weeks of age

integument

excessive hair ( J:171191 )

• mice treated with doxycycline for 6 weeks (either initiated at birth or 4 to 6 weeks of age) exhibit excessive hair growth compared with wild-type mice

progressive hair loss ( J:171191 )

• in mice treated with doxycycline beyond 20 weeks

• however, reactivation after 4 weeks of doxycycline prevents hair loss

abnormal hair follicle morphology ( J:171191 )

• in mice treated with doxycycline beyond 20 weeks

craniofacial

short snout ( J:171191 )

• in mice treated with doxycycline 1 to 2 days prior to birth

• reactivation after 4 weeks of doxycycline treatment does not rescue stunted snout

growth/size/body

short snout ( J:171191 )

• in mice treated with doxycycline 1 to 2 days prior to birth

• reactivation after 4 weeks of doxycycline treatment does not rescue stunted snout

decreased body size ( J:171191 )

• runting in mice treated with doxycycline 1 to 2 days prior to birth

postnatal growth retardation ( J:171191 )

• in mice treated with doxycycline 1 to 2 days prior to birth

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:171191 )

• in mice treated with doxycycline from 4 to 6 weeks of age

immune system

increased T cell derived lymphoma incidence ( J:171191 )

• in mice treated with doxycycline from 4 to 6 weeks of age

hematopoietic system

increased T cell derived lymphoma incidence ( J:171191 )

• in mice treated with doxycycline from 4 to 6 weeks of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
lymphoid leukemia		DOID:1037		J:171191

Genotype
MGI:5000007

cx32

• Allelic Composition: Col1a1^{tm8(tetO-GFP/RNAi:Rpa3)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:171348 )

• most mice treated with doxycycline between 5 and 10 weeks of age die prematurely

growth/size/body

weight loss ( J:171348 )

• in doxycycline-treated mice

cellular

abnormal cell cycle ( J:171348 )

• doxycycline-treated mice exhibit cell cycle arrest unlike control mice

Genotype
MGI:5000010

cx33

• Allelic Composition: Col1a1^{tm10(tetO*-RFP/RNAi:Rpa3)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

neonatal lethality, complete penetrance ( J:171348 )

• when treated in utero with doxycycline, mice die shortly after birth

cellular

abnormal cell cycle ( J:171348 )

• doxycycline-treated mouse embryonic fibroblasts arrest in S phase with increased DNA content compared with untreated cells

early cellular replicative senescence ( J:171348 )

• doxycycline-treated mouse embryonic fibroblasts exhibit early cellular replicative senescence compared with untreated cells

• however, withdrawal of doxcycline restores proliferation

normal phenotype

no abnormal phenotype detected ( J:171348 )

• mice treated with doxycycline during adulthood exhibit no abnormal phenotype

Genotype
MGI:5000011

cx34

• Allelic Composition: Col1a1^{tm10(tetO*-RFP/RNAi:Rpa3)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:171348 )

• all mice treated with doxycycline between 5 and 10 weeks of age die prematurely

digestive/alimentary system

abnormal small intestinal crypt cell physiology ( J:171348 )

• doxycycline-treated adult mice exhibit atrophy of intestinal epithelium unlike control mice

• however, withdrawal of doxycycline reverses villus atrophy

abnormal small intestinal crypt cell proliferation ( J:171348 )

• doxycycline-treated adult mice exhibit decreased proliferation and cell cycle arrest in the intestinal epithelium unlike control mice

hematopoietic system

decreased erythroid progenitor cell number ( J:171348 )

• doxycycline-treated adult mice exhibit decreased erythroid precursors in the bone marrow unlike in control mice

growth/size/body

weight loss ( J:171348 )

• in doxycycline-treated adult mice

• however, mice regain weight after withdrawal of doxycycline

cellular

abnormal small intestinal crypt cell proliferation ( J:171348 )

• doxycycline-treated adult mice exhibit decreased proliferation and cell cycle arrest in the intestinal epithelium unlike control mice

Genotype
MGI:5000012

cx35

• Allelic Composition: Col1a1^{tm11(tetO*-RFP/RNAi:Rpa3)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

neonatal lethality, complete penetrance ( J:171348 )

• when treated in utero with doxycycline, mice die shortly after birth

cellular

abnormal cell cycle ( J:171348 )

• doxycycline-treated mouse embryonic fibroblasts arrest in S phase with increased DNA content compared with untreated cells

early cellular replicative senescence ( J:171348 )

• doxycycline-treated mouse embryonic fibroblasts exhibit early cellular replicative senescence compared with untreated cells

• however, withdrawal of doxcycline restores proliferation

normal phenotype

no abnormal phenotype detected ( J:171348 )

• mice treated with doxycycline during adulthood exhibit no abnormal phenotype

Genotype
MGI:5478622

cx36

• Allelic Composition: Col1a1^{tm1(tetO-Yod1*)Hpl}/Col1a1^{tm1(tetO-Yod1*)Hpl}; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}
• Genetic Background: involves: 129S4/SvJae * C57BL/6

immune system

immune system phenotype ( J:194608 )

N • doxycycline-treated mice exhibit normal T cell distribution in lymphoid organs

abnormal CD8-positive, alpha-beta T cell physiology ( J:194608 )

• CD8+ T cells from doxycycline-treated mice exhibit enhanced response to immunization with viral infection and improved viral growth control compared with control cells

abnormal professional antigen presenting cell physiology ( J:194608 )

• following exposure to ovalbumin, antigen presenting cells (APCs) from doxycycline-treated mice exhibit enhanced antigen cross-production with increased induction of proliferation and IL2 production in OT-I cells compared with control cells

• following infection with MHV-68 and irradiation, bone marrow derived dendritic cells from doxycycline-treated mice prime more effective CD8+ T cell response compared with control cells

• APCs from doxycycline-treated mice exhibit prolonged antigen retention compared with control cells

• cross-presentation in doxycycline-treated mice requires acidification and is insensitive to brefeldin compared to in control cells

• however, antigen presentation in doxycycline-treated mice is normal

hematopoietic system

abnormal CD8-positive, alpha-beta T cell physiology ( J:194608 )

• CD8+ T cells from doxycycline-treated mice exhibit enhanced response to immunization with viral infection and improved viral growth control compared with control cells

Genotype
MGI:5485198

cx37

• Allelic Composition: Col1a1^{tm1(tetO-EWSR1/ATF1)Yasu}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:194505 )

• after 3 to 10 months of doxycycline-treated mice with median survival of 20 weeks

neoplasm

tumor regression ( J:194505 )

• in doxycycline-treated mice following withdrawal of doxycycline

increased sarcoma incidence ( J:194505 )

• in the trunks, heads, limbs, and whisker pads of all doxycycline-treated mice after 3 months arising from neural crest-lineage cells

cellular

decreased fibroblast proliferation ( J:194505 )

• in doxycycline-treated mouse embryonic fibroblasts

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
clear cell sarcoma		DOID:4233		J:194505

Genotype
MGI:5500065

cx38

• Allelic Composition: Col1a1^{tm3(tetO-Mirlet7g/Mir21)Gqda}/?; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

reproductive system

decreased primordial germ cell number ( J:196313 )

• in doxycycline-treated neonates

cellular

decreased primordial germ cell number ( J:196313 )

• in doxycycline-treated neonates

Genotype
MGI:5585616

cx39

• Allelic Composition: Col1a1^{tm1(tetO-Cyp26b1)Mfra}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

immune system

abnormal lymphatic vessel morphology ( J:206581 )

• mice treated with doxycycline at E8.5 exhibit smaller jugular lymph sac at E 14.5 compared with control mice

Genotype
MGI:5586502

cx40

• Allelic Composition: Col1a1^{tm3(tetO-Fosl1,-DsRed)Wag}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

liver/biliary system

liver fibrosis ( J:213764 )

• periportal with immune infiltrate in doxycycline-treated mice

skeleton

abnormal skeleton morphology ( J:213764 )

• in doxycycline-treated mice at necropsy

growth/size/body

weight loss ( J:213764 )

• in doxycycline-treated mice

enlarged spleen ( J:213764 )

• in doxycycline-treated mice at necropsy

behavior/neurological

lethargy ( J:213764 )

• in doxycycline-treated mice

homeostasis/metabolism

ascites ( J:213764 )

• sometimes in doxycycline-treated mice at necropsy

hematopoietic system

enlarged spleen ( J:213764 )

• in doxycycline-treated mice at necropsy

immune system

enlarged spleen ( J:213764 )

• in doxycycline-treated mice at necropsy

Genotype
MGI:5754807

cx41

• Allelic Composition: Col1a1^{tm1(tetO-U2AF1*S34F)Mjwa}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/?
• Genetic Background: involves: 129S4/SvJae * C57BL/6

hematopoietic system

abnormal definitive hematopoiesis ( J:221403 )

• lethally-irradiated mice transplanted with mutant bone marrow and treated with doxycycline exhibit altered hematopoiesis, showing peripheral blood leukopenia, and changes in the distribution of mature hematopoietic lineages in the peripheral blood and spleen (reduction in B cells and monocytes, increase in neutrophils) and an increase in the frequency of progenitor cells in the bone marrow and spleen as well as the frequency of progenitor cells that are cycling in the bone marrow

• however, lethally-irradiated mice transplanted with mutant bone marrow and treated with doxycycline do not develop myelodysplastic syndrome or acute myeloid leukemia after at least 1 year of continuous doxycycline

Genotype
MGI:5754809

cx42

• Allelic Composition: Col1a1^{tm2(tetO-U2AF1)Mjwa}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6

hematopoietic system

hematopoietic system phenotype ( J:221403 )

N • transplantation of bone marrow from mutants into lethally-irradiated recipient mice treated with doxycycline does not result in altered hematopoiesis

Genotype
MGI:3703249

cx43

• Allelic Composition: Col1a1^{tm2(tetO-Pou5f1)Jae}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:98920 )

• mice with doxycycline-induced ectopic Oct4 expression become morbid after 3-5 days of treatment and usually die after 5-10 days of treatment

• however, if doxycycline treatment is stopped after 5 days mice completely recover

digestive/alimentary system

abnormal intestinal epithelium morphology ( J:98920 )

• after doxycline treatment, dysplastic cells are found in the entire epithelium; cells have structural and cytological dysplasia which mimics adenocarcinoma

abnormal small intestine morphology ( J:98920 )

• the proximal part of the small intestine is most severely affected by doxycycline treatment with abnormal cells often almost obstructing the lumen

• after 5 days of doxycycline treatment, proliferative zone expands; postmitotic, differentiated cells lining the villus are replaced

• upon cessation of treatment, cells migrate to final destinations and differentiate resulting in restoration of normal morphology

abnormal forestomach morphology ( J:98920 )

• in doxycycline treated mice, cells in the forestomach show a marked atypia and increased mitotic activity

abnormal stomach mucosa morphology ( J:98920 )

• pyloric mucosa contains lesions resembling high grade-dysplasia in doxycycline treated mice

abnormal intermediate gastric gland morphology ( J:98920 )

• hyperplastic fundic glands are seen in doxycycline treated mice

abnormal stomach epithelium morphology ( J:98920 )

• in doxycycline treated mice, forestomach epithelium is thickened and stomach shows lack of differentiation into granular and cornified cell layers compared to control mice

• the thickened epithelium consists of atypical cells with enlarged nuclei and prominent nucleoli

abnormal stomach glandular epithelium morphology ( J:98920 )

• after doxycycline treatment, mice display severe dysplasia and increased proliferation

stomach epithelial hyperplasia ( J:98920 )

• cells show atypia and increased mitotic activity throughout the squamous epithelial layer in doxycycline treated mice

homeostasis/metabolism

dehydration ( J:98920 )

• after 3-5 days of doxycycline treatment, animals display severe dehydration

cellular

abnormal cell proliferation ( J:98920 )

• abnormal cell proliferation is observed in several organs after 2 days of Oct4-induction

• however, complete reversion is seen with withdrawal of doxycycline treatment

behavior/neurological

lethargy ( J:98920 )

• animals become lethargic with doxycycline treatment within 3-5 days

hematopoietic system

thymus atrophy ( J:98920 )

• atrophy and absence of CD4, CD8 double positive cells in doxycycline treated mice

spleen atrophy ( J:98920 )

• in doxycycline treated mice

immune system

thymus atrophy ( J:98920 )

• atrophy and absence of CD4, CD8 double positive cells in doxycycline treated mice

spleen atrophy ( J:98920 )

• in doxycycline treated mice

neoplasm

increased skin tumor incidence ( J:98920 )

• in doxycycline treated mice, tumors originating from the outer-root-sheath progenitors and invading the subcutaneous layer are seen

integument

abnormal hair follicle morphology ( J:98920 )

• increased numbers of immature cells in the hair follicles of the skin are seen after 5-10 days of doxycycline

abnormal epidermal layer morphology ( J:98920 )

• after 5-10 days of doxycycline treatment, mice show mild to moderate epidermal dysplasia with a decrease in differentiation in dysplastic cells

increased skin tumor incidence ( J:98920 )

• in doxycycline treated mice, tumors originating from the outer-root-sheath progenitors and invading the subcutaneous layer are seen

endocrine/exocrine glands

abnormal intermediate gastric gland morphology ( J:98920 )

• hyperplastic fundic glands are seen in doxycycline treated mice

thymus atrophy ( J:98920 )

• atrophy and absence of CD4, CD8 double positive cells in doxycycline treated mice

Genotype
MGI:5911575

cx44

• Allelic Composition: Col1a1^{tm1(tetO-GFP/RNAi:Rad21)Iaai}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

hematopoietic system

abnormal definitive hematopoiesis ( J:229031 )

• lineage skewing is seen following prolonged doxycycline exposure (30 days)

extramedullary hematopoiesis ( J:229031 )

• in the splenic parenchyma

abnormal bone marrow cell number ( J:229031 )

• decrease in the Ter119+ cell population

decreased B cell number ( J:229031 )

• decrease in the proportion of B cell population (B220+)

increased myeloid cell number ( J:229031 )

• increase in the proportion of myelomonocytic (Cd11b+/Gr1+) and erythroid (CD71+/Ter119+) cells

• increased amount of early erythroid (CD71+/Ter119+) cells in the spleen

abnormal hematopoietic stem cell morphology ( J:229031 )

• increase in nuclear size in sorted Lineage-/c-Kit+ progenitor cells not associated with an increase of genomic material or instability

increased hematopoietic stem cell number ( J:229031 )

• in the spleen

immune system

decreased B cell number ( J:229031 )

• decrease in the proportion of B cell population (B220+)

Genotype
MGI:5911576

cx45

• Allelic Composition: Col1a1^{tm2(tetO-GFP/RNAi:Smc1a)Iaai}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

hematopoietic system

enlarged spleen ( J:229031 )

abnormal definitive hematopoiesis ( J:229031 )

• lineage skewing is seen following prolonged doxycycline exposure (30 days)

myeloid metaplasia ( J:229031 )

extramedullary hematopoiesis ( J:229031 )

• in the splenic parenchyma

abnormal bone marrow cell number ( J:229031 )

• decrease in the Ter119+ cell population

increased bone marrow cell number ( J:229031 )

• hypercellular bone marrow with erythroid and megakaryocytic hypoplasia and marked myeloid hyperplasia

increased granulocyte monocyte progenitor cell number ( J:229031 )

• in the GFP+ cells in the bone marrow

increased neutrophil cell number ( J:229031 )

• in peripheral blood of aged mice

decreased B cell number ( J:229031 )

• decrease in the proportion of B cell population (B220+)

increased myeloid cell number ( J:229031 )

• increase in the proportion of myelomonocytic (Cd11b+/Gr1+) and erythroid (CD71+/Ter119+) cells

• increased amount of early erythroid (CD71+/Ter119+) cells in the spleen

myeloid hyperplasia ( J:229031 )

• aged mice show marked expansion of myeloid elements (granulocytic > monocytic) in the peripheral blood

abnormal hematopoietic stem cell morphology ( J:229031 )

• increase in nuclear size in sorted Lineage-/c-Kit+ progenitor cells not associated with an increase of genomic material or instability

decreased hematopoietic stem cell number ( J:229031 )

• decrease in the number of GFP+ cells in the long-term (CD150+) and short-term (CD150-/CD48-) subsets

• compensated for with an increase in the CD150+/CD48+ multipotent progenitor subset

increased hematopoietic stem cell number ( J:229031 )

• in the spleen

increased spleen red pulp amount ( J:229031 )

• in aged mice

immune system

enlarged spleen ( J:229031 )

myeloid hyperplasia ( J:229031 )

• aged mice show marked expansion of myeloid elements (granulocytic > monocytic) in the peripheral blood

myeloid metaplasia ( J:229031 )

increased neutrophil cell number ( J:229031 )

• in peripheral blood of aged mice

decreased B cell number ( J:229031 )

• decrease in the proportion of B cell population (B220+)

increased spleen red pulp amount ( J:229031 )

• in aged mice

growth/size/body

enlarged spleen ( J:229031 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
myeloproliferative neoplasm		DOID:2226		J:229031

Genotype
MGI:5911578

cx46

• Allelic Composition: Col1a1^{tm3(tetO-GFP/RNAi:Stag2)Iaai}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

hematopoietic system

abnormal definitive hematopoiesis ( J:229031 )

• lineage skewing is seen following prolonged doxycycline exposure (30 days)

decreased B cell number ( J:229031 )

• decrease in the proportion of B cell population (B220+)

increased myeloid cell number ( J:229031 )

• increase in the proportion of myelomonocytic (Cd11b+/Gr1+) and erythroid (CD71+/Ter119+) cells

abnormal hematopoietic stem cell morphology ( J:229031 )

• increase in nuclear size in sorted Lineage-/c-Kit+ progenitor cells not associated with an increase of genomic material or instability

decreased hematopoietic stem cell number ( J:229031 )

• decrease in the number of GFP+ cells in the long-term (CD150+) and short-term (CD150-/CD48-) subsets

immune system

decreased B cell number ( J:229031 )

• decrease in the proportion of B cell population (B220+)

Genotype
MGI:5911579

cx47

• Allelic Composition: Col1a1^{tm2(tetO-GFP/RNAi:Smc1a)Iaai}/Col1a1^{tm3(tetO-GFP/RNAi:Stag2)Iaai}; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

hematopoietic system

abnormal definitive hematopoiesis ( J:229031 )

• lineage skewing is seen following short term doxycycline exposure

myeloid hyperplasia ( J:229031 )

• develops over time

anemia ( J:229031 )

• develops over time

decreased B cell number ( J:229031 )

• decrease in the proportion of B cell population (B220+) develops over time

abnormal spleen morphology ( J:229031 )

• disrupted morphology

enlarged spleen ( J:229031 )

• following short term doxycycline exposure

immune system

myeloid hyperplasia ( J:229031 )

• develops over time

decreased B cell number ( J:229031 )

• decrease in the proportion of B cell population (B220+) develops over time

abnormal spleen morphology ( J:229031 )

• disrupted morphology

enlarged spleen ( J:229031 )

• following short term doxycycline exposure

growth/size/body

enlarged spleen ( J:229031 )

• following short term doxycycline exposure

Genotype
MGI:5474007

cx48

• Allelic Composition: Col1a1^{tm2(tetO-CTNNB1*)Hoch}/Col1a1^{tm2(tetO-CTNNB1*)Hoch}; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/?
• Genetic Background: involves: 129S4/SvJae * C57BL/6

digestive/alimentary system

abnormal intestinal goblet cell morphology ( J:191050 )

• suppressed cellular differentiation toward goblet cells

abnormal intestinal epithelium morphology ( J:191050 )

• after doxycycline treatment of adults

• number of intestinal stem cells is increased

• decreased cell division in colonic cells

abnormal crypts of Lieberkuhn morphology ( J:191050 )

• crypt fission and budding is normalized after treatment with notch inhibitors

abnormal large intestine crypts of Lieberkuhn morphology ( J:191050 )

• crypt fission is often observed in the large intestine

abnormal small intestine crypts of Lieberkuhn morphology ( J:191050 )

• crypt fission is often observed in the small intestine

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:191050 )

• crypt fission and budding is normalized after treatment with notch inhibitors

abnormal large intestine crypts of Lieberkuhn morphology ( J:191050 )

• crypt fission is often observed in the large intestine

abnormal small intestine crypts of Lieberkuhn morphology ( J:191050 )

• crypt fission is often observed in the small intestine

cellular

abnormal intestinal goblet cell morphology ( J:191050 )

• suppressed cellular differentiation toward goblet cells

Genotype
MGI:5313423

cx49

• Allelic Composition: Apc^Min/Apc⁺; Col1a1^{tm12(tetO-Dnmt3a_i1)Jae}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

neoplasm

neoplasm ( J:127808 )

N • doxycycline-treated mice develop intestinal adenomas at the same rate as in Apc^min heterozygotes

Genotype
MGI:5437856

cx50

• Allelic Composition: Col1a1^{tm1(tetO-Deptor)Dmsa}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/?
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

homeostasis/metabolism

increased susceptibility to diet-induced obesity ( J:187378 )

• doxycycline treated mice gain more weight on a high fat diet; not caused by a difference in food intake or locomotion

increased circulating leptin level ( J:187378 )

• in doxycycline treated mice on a high fat diet

increased triglyceride level ( J:187378 )

• MEFs treated with doxycycline and differentiated in adipocytes show increased triglyceride accumulation

adipose tissue

increased white adipose tissue amount ( J:187378 )

• in doxycycline treated mice on a high fat diet

liver/biliary system

increased liver weight ( J:187378 )

• in doxycycline treated mice on a high fat diet

hepatic steatosis ( J:187378 )

• in doxycycline treated mice on a high fat diet

growth/size/body

increased susceptibility to diet-induced obesity ( J:187378 )

• doxycycline treated mice gain more weight on a high fat diet; not caused by a difference in food intake or locomotion

increased liver weight ( J:187378 )

• in doxycycline treated mice on a high fat diet

Genotype
MGI:5313419

cx51

• Allelic Composition: Apc^Min/Apc⁺; Col1a1^{tm9(tetO-Dnmt3b_i1)Jae}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:127808 )

• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apc^min heterozygotes

increased tumor growth/size ( J:127808 )

• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apc^min heterozygotes

• doxycycline-treated mice exhibit increased size of microadenomas compared with Apc^min heterozygotes

cellular

abnormal DNA methylation ( J:127808 )

• doxycycline-treated mice exhibit loss of imprinting and increased expression of Igf2 compared with control mice

• doxycycline-treated mice exhibit biallelic methylation of H19 differentially methylated region in tumors and normal colon epithelial cells compared with control mice

• doxycycline-treated mice exhibit hypermethylation of Sfrp2, Sfrp4 and Sfrp5 in tumors and normal colon epithelial cells unlike control mice

• however, mice exhibit normal methylation of of Snrpn differentially methylated region in tumors and normal colon epithelial cells, and global DNA methylation

digestive/alimentary system

increased intestinal adenoma incidence ( J:127808 )

• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apc^min heterozygotes

Genotype
MGI:5313421

cx52

• Allelic Composition: Apc^Min/Apc⁺; Col1a1^{tm11(tetO-Dnmt3b_i6)Jae}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

neoplasm

neoplasm ( J:127808 )

N • doxycycline-treated mice develop intestinal adenomas at the same rate as in Apc^min heterozygotes

Genotype
MGI:5313420

cx53

• Allelic Composition: Apc^Min/Apc⁺; Col1a1^{tm10(tetO-Dnmt3b_i3)Jae}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

neoplasm

neoplasm ( J:127808 )

N • doxycycline-treated mice develop intestinal adenomas at the same rate as in Apc^min heterozygotes

Genotype
MGI:5469373

cx54

• Allelic Composition: Col1a1^{tm1(tetO-CTNNB1)Tcd}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

digestive/alimentary system

digestive/alimentary phenotype ( J:193365 )

N • doxycycline-treated mice exhibit normal villus compartment

abnormal enterocyte apoptosis ( J:193365 )

• docycycline-treated mice exhibit apoptosis all along the enlarged crypt axis instead of being restricted to the bottom of the crypt as in control mice

increased enterocyte apoptosis ( J:193365 )

• upon withdrawal of doxycycline

abnormal enterocyte proliferation ( J:193365 )

• increased in the crypt compartment of doxycycline-treated mice

abnormal intestine development ( J:193365 )

• doxycycline-treated mice exhibit partially altered intestinal differentiation compared with control mice

abnormal crypts of Lieberkuhn morphology ( J:193365 )

• enlarged crypts in doxycycline-treated mice

• however, withdrawal of doxycycline leads to a rapid regression of the crypt compartment

growth/size/body

decreased body weight ( J:193365 )

• in docycycline-treated mice

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:193365 )

• enlarged crypts in doxycycline-treated mice

• however, withdrawal of doxycycline leads to a rapid regression of the crypt compartment

cellular

abnormal enterocyte apoptosis ( J:193365 )

• docycycline-treated mice exhibit apoptosis all along the enlarged crypt axis instead of being restricted to the bottom of the crypt as in control mice

increased enterocyte apoptosis ( J:193365 )

• upon withdrawal of doxycycline

abnormal enterocyte proliferation ( J:193365 )

• increased in the crypt compartment of doxycycline-treated mice

Genotype
MGI:6446222

cx55

• Allelic Composition: Btnl1^tm1(KOMP)Mbp/Btnl1^tm1(KOMP)Mbp; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/0; Tg(tetO-Btnl1)#Ahay/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6N

hematopoietic system

decreased gamma-delta intraepithelial T cell number ( J:236526 )

• 90% loss of TCRVgamma7+ intraepithelial lymphocytes (IELs) in the gut with or without doxycycline administration

• almost total loss of TCRVgamma7GL2+ IELs in the gut with or without doxycycline administration

• normal CD122hi TCRVgamma7+ IELs (most also Ki67+) in the gut after doxycycline administration

immune system

decreased gamma-delta intraepithelial T cell number ( J:236526 )

• 90% loss of TCRVgamma7+ intraepithelial lymphocytes (IELs) in the gut with or without doxycycline administration

• almost total loss of TCRVgamma7GL2+ IELs in the gut with or without doxycycline administration

• normal CD122hi TCRVgamma7+ IELs (most also Ki67+) in the gut after doxycycline administration

Genotype
MGI:5294614

cx56

• Allelic Composition: Col1a1^{tm2(tetO-LIN28B)Gqda}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * CD-1

growth/size/body

decreased susceptibility to diet-induced obesity ( J:177113 )

• following doxycycline treatment mice gain less weight when fed a high fat diet compared to wild-type mice

homeostasis/metabolism

decreased susceptibility to diet-induced obesity ( J:177113 )

• following doxycycline treatment mice gain less weight when fed a high fat diet compared to wild-type mice

hypoglycemia ( J:177113 )

• following doxycycline treatment average fasting glucose is less than 50 mg/dL

improved glucose tolerance ( J:177113 )

• following doxycycline treatment on a normal or high fat diet

increased insulin sensitivity ( J:177113 )

• following doxycycline treatment

Genotype
MGI:5294615

cx57

• Allelic Composition: Col1a1^{tm3(tetO-Mirlet7g/Mir21)Gqda}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * CD-1

growth/size/body

decreased body size ( J:177113 )

• following doxycycline treatment

postnatal growth retardation ( J:177113 )

• following doxycycline treatment

homeostasis/metabolism

increased circulating glucose level ( J:177113 )

• in the fed state following doxycycline treatment

increased circulating insulin level ( J:177113 )

• during a glucose tolerance test in doxycycline treated mice

• however, no difference in insulin sensitivity is detected following doxycycline treatment

impaired glucose tolerance ( J:177113 )

• following doxycycline treatment on a normal or high fat diet

Genotype
MGI:5294616

cx58

• Allelic Composition: Col1a1^{tm2(tetO-LIN28B)Gqda}/Col1a1^{tm3(tetO-Mirlet7g/Mir21)Gqda}; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * CD-1

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:177113 )

N • following doxycycline treatment responses in a glucose tolerance test are similar to controls

Genotype
MGI:5000009

cx59

• Allelic Composition: Col1a1^{tm10(tetO*-RFP/RNAi:Rpa3)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺; Tg(CMV-rtTA)4Bjd/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * NMRI

mortality/aging

premature death ( J:171348 )

• most mice treated with doxycycline between 5 and 10 weeks of age die prematurely

growth/size/body

weight loss ( J:171348 )

• in doxycycline-treated mice

Genotype
MGI:5000006

cx60

• Allelic Composition: Col1a1^{tm8(tetO-GFP/RNAi:Rpa3)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺; Tg(CMV-rtTA)4Bjd/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * NMRI

mortality/aging

premature death ( J:171348 )

• half of mice treated with doxycycline between 5 and 10 weeks of age die prematurely

growth/size/body

weight loss ( J:171348 )

• in doxycycline-treated mice

cellular

abnormal cell cycle ( J:171348 )

• doxycycline-treated mice exhibit cell cycle arrest in the liver, spleen, and intestine unlike control mice

Genotype
MGI:5000014

cx61

• Allelic Composition: Col1a1^{tm11(tetO*-RFP/RNAi:Rpa3)Slowe}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺; Tg(CMV-rtTA)4Bjd/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * NMRI

mortality/aging

premature death ( J:171348 )

• most mice treated with doxycycline between 5 and 10 weeks of age die prematurely

growth/size/body

weight loss ( J:171348 )

• in doxycycline-treated mice

Genotype
MGI:5698051

cx62

• Allelic Composition: Col1a1^{tm1(tetO-Stat1)Biat}/Col1a1^{tm1(tetO-Stat1)Biat}; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}; Stat1^tm1Dlv/Stat1^tm1Dlv
• Genetic Background: involves: 129S/SvEv * 129S4/SvJae * C57BL/6

mortality/aging

abnormal susceptibility to infection induced morbidity/mortality ( J:212694 )

• Vesicular Stomatitis Virus or Encephalomyocarditis Virus infection results in death

• mice treated with doxycycline prior to viral infection survive at rates only slightly lower than wild-type controls

immune system

abnormal susceptibility to infection induced morbidity/mortality ( J:212694 )

• Vesicular Stomatitis Virus or Encephalomyocarditis Virus infection results in death

• mice treated with doxycycline prior to viral infection survive at rates only slightly lower than wild-type controls