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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gt(ROSA)26Sortm1(rtTA*M2)Jae
targeted mutation 1, Rudolf Jaenisch
MGI:3702294
Summary 61 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Rr96tm1.1Tich/Rr96+
Gt(ROSA)26Sortm1(cre/ERT2)Thl/Gt(ROSA)26Sortm1(rtTA*M2)Jae
involves: 129 * 129S4/SvJae * C57BL/6 MGI:5470231
cn2
Acvr1tm2.1Vlcg/Acvr1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(tetO-cre)1Jaw/0
involves: 129 * 129S4/SvJae * C57BL/6 * C57BL/6NTac MGI:5881968
cn3
Col1a1tm2(tetO-IDH2*R140Q)Ppp/Col1a1tm2(tetO-IDH2*R140Q)Ppp
Flt3tm1.1Dosm/Flt3tm1.1Dosm
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?
involves: 129 * C57BL/6 MGI:5697542
cn4
Col1a1tm5(tetO-GFP/RNAi:Cdkn2a)Slowe/Col1a1+
Gt(ROSA)26Sortm1(Luc)Kael/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Krastm4Tyj/Kras+
Tg(Scgb1a1-rtTA)1Jaw/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 MGI:4999988
cn5
Col1a1tm1(tetO-EWSR1/ATF1)Yasu/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(EYFP)Cos
Tg(Mpz-cre)94Imeg/0
involves: 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:5485201
cn6
Col1a1tm2(tetO-IDH2*R140Q)Ppp/Col1a1tm2(tetO-IDH2*R140Q)Ppp
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?
involves: 129S4/SvJae * C57BL/6 MGI:5697539
cn7
Col1a1tm17(tetO-GFP,-cas9*)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5755868
cn8
Col1a1tm18(tetO-GFP,-cas9*)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5755878
cn9
Col1a1tm19(tetO-GFP,-cas9*)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5755879
cn10
Col1a1tm20(tetO-GFP,-cas9*D10A)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5755882
cn11
Col1a1tm1(tetO-EWSR1/ATF1)Yasu/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
H2az2Tg(Wnt1-cre)11Rth/H2az2+
Tg(CAG-cat,-lacZ)11Miya/0
involves: 129S4/SvJae * C57BL/6 * CBA/J * DBA/2 MGI:5485200
cx12
Col1a1tm9(tetO-GFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
chimera involves: 129S4/SvJae * C57BL/6 MGI:5000008
cx13
Rr96tm1.1Tich/Rr96+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129 * 129S4/SvJae * C57BL/6 MGI:5470229
cx14
Rr96tm1.1Tich/Rr96tm1.1Tich
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
involves: 129 * 129S4/SvJae * C57BL/6 MGI:5470230
cx15
Col1a1tm1(tetO-Irf4)Sing/Col1a1tm1(tetO-Irf4)Sing
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Irf4tm1Mak/Irf4tm1Mak
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5529094
cx16
Col1a1tm1(tetO-Irf4)Sing/Col1a1tm1(tetO-Irf4)Sing
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Irf4tm1Mak/Irf4+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5529093
cx17
Col1a1tm1(tetO-Yod1*)Hpl/Col1a1tm1(tetO-Yod1*)Hpl
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Tap1tm1Arp/Tap1tm1Arp
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 MGI:5478623
cx18
Col1a1tm8(tetO-GFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
involves: 129S4/SvJae * C57BL/6 MGI:5000007
cx19
Col1a1tm10(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5000010
cx20
Col1a1tm10(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
involves: 129S4/SvJae * C57BL/6 MGI:5000011
cx21
Col1a1tm11(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5000012
cx22
Col1a1tm11(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
involves: 129S4/SvJae * C57BL/6 MGI:5000013
cx23
Col1a1tm1(tetO-Tcfap2c)Hsc/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5051636
cx24
Col1a1tm1(tetO-RNAi:Rps19)Karl/Col1a1tm1(tetO-RNAi:Rps19)Karl
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
involves: 129S4/SvJae * C57BL/6 MGI:5304756
cx25
Col1a1tm1(tetO-RNAi:Rps19)Karl/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
involves: 129S4/SvJae * C57BL/6 MGI:5304757
cx26
Col1a1tm2(tetO-RNAi:Rps19)Karl/Col1a1tm2(tetO-RNAi:Rps19)Karl
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
involves: 129S4/SvJae * C57BL/6 MGI:5304758
cx27
Col1a1tm2(tetO-RNAi:Rps19)Karl/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
involves: 129S4/SvJae * C57BL/6 MGI:5304759
cx28
Col1a1tm2(tetO-Pou5f1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:3703249
cx29
Col1a1tm3(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae/Col1a1tm3(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
involves: 129S4/SvJae * C57BL/6 MGI:4430610
cx30
Col1a1tm6(tetO-MSI2)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:4822382
cx31
Col1a1tm1(tetO-GFP/RNAi:luc)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:4999980
cx32
Col1a1tm3(tetO-GFP/RNAi:Apc)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:4999985
cx33
Col1a1tm4(tetO-GFP/RNAi:Apc)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:4999987
cx34
Col1a1tm1(tetO-Yod1*)Hpl/Col1a1tm1(tetO-Yod1*)Hpl
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
involves: 129S4/SvJae * C57BL/6 MGI:5478622
cx35
Col1a1tm1(tetO-EWSR1/ATF1)Yasu/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5485198
cx36
Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda/?
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5500065
cx37
Col1a1tm1(tetO-Cyp26b1)Mfra/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5585616
cx38
Col1a1tm3(tetO-Fosl1,-DsRed)Wag/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5586502
cx39
Col1a1tm1(tetO-U2AF1*S34F)Mjwa/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?
involves: 129S4/SvJae * C57BL/6 MGI:5754807
cx40
Col1a1tm2(tetO-U2AF1)Mjwa/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/0
involves: 129S4/SvJae * C57BL/6 MGI:5754809
cx41
Col1a1tm1(tetO-GFP/RNAi:Rad21)Iaai/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5911575
cx42
Col1a1tm2(tetO-GFP/RNAi:Smc1a)Iaai/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5911576
cx43
Col1a1tm3(tetO-GFP/RNAi:Stag2)Iaai/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5911578
cx44
Col1a1tm2(tetO-GFP/RNAi:Smc1a)Iaai/Col1a1tm3(tetO-GFP/RNAi:Stag2)Iaai
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5911579
cx45
Col1a1tm1(tetO-YAP1*)Fcam/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5316663
cx46
Col1a1tm1(tetO-Yap1*)Lrsn/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 MGI:5430595
cx47
Col1a1tm2(tetO-CTNNB1*)Hoch/Col1a1tm2(tetO-CTNNB1*)Hoch
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?
involves: 129S4/SvJae * C57BL/6 MGI:5474007
cx48
ApcMin/Apc+
Col1a1tm10(tetO-Dnmt3b_i3)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5313420
cx49
ApcMin/Apc+
Col1a1tm12(tetO-Dnmt3a_i1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5313423
cx50
ApcMin/Apc+
Col1a1tm9(tetO-Dnmt3b_i1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5313419
cx51
Col1a1tm1(tetO-Deptor)Dmsa/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5437856
cx52
Col1a1tm1(tetO-CTNNB1)Tcd/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5469373
cx53
ApcMin/Apc+
Col1a1tm11(tetO-Dnmt3b_i6)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5313421
cx54
Btnl1tm1(KOMP)Mbp/Btnl1tm1(KOMP)Mbp
Gt(ROSA)26Sortm1(rtTA*M2)Jae/0
Tg(tetO-Btnl1)#Ahay/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6N MGI:6446222
cx55
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 * CD-1 MGI:5294614
cx56
Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 * CD-1 MGI:5294615
cx57
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 * CD-1 MGI:5294616
cx58
Col1a1tm10(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(CMV-rtTA)4Bjd/0
involves: 129S4/SvJae * C57BL/6 * NMRI MGI:5000009
cx59
Col1a1tm11(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(CMV-rtTA)4Bjd/0
involves: 129S4/SvJae * C57BL/6 * NMRI MGI:5000014
cx60
Col1a1tm8(tetO-GFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(CMV-rtTA)4Bjd/0
involves: 129S4/SvJae * C57BL/6 * NMRI MGI:5000006
cx61
Col1a1tm1(tetO-Stat1)Biat/Col1a1tm1(tetO-Stat1)Biat
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Stat1tm1Dlv/Stat1tm1Dlv
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 MGI:5698051


Genotype
MGI:5470231
cn1
Allelic
Composition
Rr96tm1.1Tich/Rr96+
Gt(ROSA)26Sortm1(cre/ERT2)Thl/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Genetic
Background
involves: 129 * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT2)Thl mutation (0 available); any Gt(ROSA)26Sor mutation (992 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Rr96tm1.1Tich mutation (0 available); any Rr96 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• derepression of Cd4 occurs in all CD4- T cells
• T cell expression of CD4 increases rapidly after cre activation

hematopoietic system
• derepression of Cd4 occurs in all CD4- T cells
• T cell expression of CD4 increases rapidly after cre activation




Genotype
MGI:5881968
cn2
Allelic
Composition
Acvr1tm2.1Vlcg/Acvr1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(tetO-cre)1Jaw/0
Genetic
Background
involves: 129 * 129S4/SvJae * C57BL/6 * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acvr1tm2.1Vlcg mutation (0 available); any Acvr1 mutation (44 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Tg(tetO-cre)1Jaw mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• 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
• 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
cn3
Allelic
Composition
Col1a1tm2(tetO-IDH2*R140Q)Ppp/Col1a1tm2(tetO-IDH2*R140Q)Ppp
Flt3tm1.1Dosm/Flt3tm1.1Dosm
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-IDH2*R140Q)Ppp mutation (1 available); any Col1a1 mutation (163 available)
Flt3tm1.1Dosm mutation (0 available); any Flt3 mutation (90 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice treated with doxycycline develop acute leukemias

mortality/aging
• reduced overall survival of doxycycline treated mice to 229 days vs 352 days for Flt3tm1.1Dosm controls




Genotype
MGI:4999988
cn4
Allelic
Composition
Col1a1tm5(tetO-GFP/RNAi:Cdkn2a)Slowe/Col1a1+
Gt(ROSA)26Sortm1(Luc)Kael/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Krastm4Tyj/Kras+
Tg(Scgb1a1-rtTA)1Jaw/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm5(tetO-GFP/RNAi:Cdkn2a)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(Luc)Kael mutation (3 available); any Gt(ROSA)26Sor mutation (992 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Scgb1a1-rtTA)1Jaw mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice treated with a cre-expressing adenovirus and treated with doxycycline exhibit reduced survival compared with control mice

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

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

growth/size/body
• in mice treated with a cre-expressing adenovirus and treated with doxycycline




Genotype
MGI:5485201
cn5
Allelic
Composition
Col1a1tm1(tetO-EWSR1/ATF1)Yasu/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(EYFP)Cos
Tg(Mpz-cre)94Imeg/0
Genetic
Background
involves: 129S4/SvJae * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-EWSR1/ATF1)Yasu mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (992 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Tg(Mpz-cre)94Imeg mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• in of all doxycycline-treated mice arising from neural crest-lineage cells




Genotype
MGI:5697539
cn6
Allelic
Composition
Col1a1tm2(tetO-IDH2*R140Q)Ppp/Col1a1tm2(tetO-IDH2*R140Q)Ppp
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-IDH2*R140Q)Ppp mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• modified IDH2 expression induced by doxycycline in chow starting around 3 weeks
• 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
• 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
• by 7 months KSL cells are increased in bone marrow relative to controls
• long-term hematopoietic stem cells also tend to expand in number
• about 1.3X larger than control spleens
• significant extramedullary hematopoiesis

neoplasm
N
• no mice on doxycycline treatment for 1 year develop leukemia
• 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
• 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
• 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
• about 1.3X larger than control spleens

growth/size/body
• about 1.3X larger than control spleens




Genotype
MGI:5755868
cn7
Allelic
Composition
Col1a1tm17(tetO-GFP,-cas9*)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm17(tetO-GFP,-cas9*)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• increased in doxycycline-treated mice
• doxycycline-treated mice exhibit dramatic hyper-proliferation and crypt expansion, blocked differentiation and ectopic Paneth cell production compared with control mice
• increased in doxycycline-treated mice

endocrine/exocrine glands
• increased in doxycycline-treated mice

cellular
• increased in doxycycline-treated mice




Genotype
MGI:5755878
cn8
Allelic
Composition
Col1a1tm18(tetO-GFP,-cas9*)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm18(tetO-GFP,-cas9*)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• doxycycline-treated mice exhibit normal crypt proliferation, differentiation and Paneth cell production




Genotype
MGI:5755879
cn9
Allelic
Composition
Col1a1tm19(tetO-GFP,-cas9*)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm19(tetO-GFP,-cas9*)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• increased in doxycycline-treated mice
• doxycycline-treated mice exhibit dramatic hyper-proliferation and crypt expansion, blocked differentiation and ectopic Paneth cell production compared with control mice
• increased in doxycycline-treated mice

cellular
• increased in doxycycline-treated mice

endocrine/exocrine glands
• increased in doxycycline-treated mice




Genotype
MGI:5755882
cn10
Allelic
Composition
Col1a1tm20(tetO-GFP,-cas9*D10A)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm20(tetO-GFP,-cas9*D10A)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• increased in doxycycline-treated mice
• doxycycline-treated mice exhibit dramatic hyper-proliferation and crypt expansion, blocked differentiation and ectopic Paneth cell production compared with control mice
• increased in doxycycline-treated mice

cellular
• increased in doxycycline-treated mice

endocrine/exocrine glands
• increased in doxycycline-treated mice




Genotype
MGI:5485200
cn11
Allelic
Composition
Col1a1tm1(tetO-EWSR1/ATF1)Yasu/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
H2az2Tg(Wnt1-cre)11Rth/H2az2+
Tg(CAG-cat,-lacZ)11Miya/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA/J * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-EWSR1/ATF1)Yasu mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
H2az2Tg(Wnt1-cre)11Rth mutation (2 available); any H2az2 mutation (26 available)
Tg(CAG-cat,-lacZ)11Miya mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• in of all doxycycline-treated mice arising from neural crest-lineage cells




Genotype
MGI:5000008
cx12
Allelic
Composition
Col1a1tm9(tetO-GFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
chimera involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm9(tetO-GFP/RNAi:Rpa3)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• the founder mouse is sterile




Genotype
MGI:5470229
cx13
Allelic
Composition
Rr96tm1.1Tich/Rr96+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129 * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Rr96tm1.1Tich mutation (0 available); any Rr96 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• 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
• 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
cx14
Allelic
Composition
Rr96tm1.1Tich/Rr96tm1.1Tich
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Genetic
Background
involves: 129 * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Rr96tm1.1Tich mutation (0 available); any Rr96 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• 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
• 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:5529094
cx15
Allelic
Composition
Col1a1tm1(tetO-Irf4)Sing/Col1a1tm1(tetO-Irf4)Sing
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Irf4tm1Mak/Irf4tm1Mak
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-Irf4)Sing mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Irf4tm1Mak mutation (2 available); any Irf4 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination but not as severe as in mice heterozygous for Irf4tm1Mak
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination but not as severe as in mice heterozygous for Irf4tm1Mak

immune system
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination but not as severe as in mice heterozygous for Irf4tm1Mak
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination but not as severe as in mice heterozygous for Irf4tm1Mak




Genotype
MGI:5529093
cx16
Allelic
Composition
Col1a1tm1(tetO-Irf4)Sing/Col1a1tm1(tetO-Irf4)Sing
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Irf4tm1Mak/Irf4+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-Irf4)Sing mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Irf4tm1Mak mutation (2 available); any Irf4 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination

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




Genotype
MGI:5478623
cx17
Allelic
Composition
Col1a1tm1(tetO-Yod1*)Hpl/Col1a1tm1(tetO-Yod1*)Hpl
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Tap1tm1Arp/Tap1tm1Arp
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-Yod1*)Hpl mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Tap1tm1Arp mutation (4 available); any Tap1 mutation (51 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• APCs from doxycycline-treated mice exhibit enhanced antigen cross-presentation compared with control cells




Genotype
MGI:5000007
cx18
Allelic
Composition
Col1a1tm8(tetO-GFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm8(tetO-GFP/RNAi:Rpa3)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mice treated with doxycycline between 5 and 10 weeks of age die prematurely

growth/size/body
• in doxycycline-treated mice

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




Genotype
MGI:5000010
cx19
Allelic
Composition
Col1a1tm10(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm10(tetO*-RFP/RNAi:Rpa3)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• when treated in utero with doxycycline, mice die shortly after birth

cellular
• doxycycline-treated mouse embryonic fibroblasts arrest in S phase with increased DNA content compared with untreated cells
• doxycycline-treated mouse embryonic fibroblasts exhibit early cellular replicative senescence compared with untreated cells
• however, withdrawal of doxcycline restores proliferation

normal phenotype
• mice treated with doxycycline during adulthood exhibit no abnormal phenotype




Genotype
MGI:5000011
cx20
Allelic
Composition
Col1a1tm10(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm10(tetO*-RFP/RNAi:Rpa3)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice treated with doxycycline between 5 and 10 weeks of age die prematurely

digestive/alimentary system
• doxycycline-treated adult mice exhibit atrophy of intestinal epithelium unlike control mice
• however, withdrawal of doxycycline reverses villus atrophy
• doxycycline-treated adult mice exhibit decreased proliferation and cell cycle arrest in the intestinal epithelium unlike control mice

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

growth/size/body
• in doxycycline-treated adult mice
• however, mice regain weight after withdrawal of doxycycline

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




Genotype
MGI:5000012
cx21
Allelic
Composition
Col1a1tm11(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm11(tetO*-RFP/RNAi:Rpa3)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• when treated in utero with doxycycline, mice die shortly after birth

cellular
• doxycycline-treated mouse embryonic fibroblasts arrest in S phase with increased DNA content compared with untreated cells
• doxycycline-treated mouse embryonic fibroblasts exhibit early cellular replicative senescence compared with untreated cells
• however, withdrawal of doxcycline restores proliferation

normal phenotype
• mice treated with doxycycline during adulthood exhibit no abnormal phenotype




Genotype
MGI:5000013
cx22
Allelic
Composition
Col1a1tm11(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm11(tetO*-RFP/RNAi:Rpa3)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice treated with doxycycline between 5 and 10 weeks of age die prematurely

digestive/alimentary system
• doxycycline-treated adult mice exhibit atrophy of intestinal epithelium unlike control mice
• however, withdrawal of doxycycline reverses villus atrophy
• doxycycline-treated adult mice exhibit decreased proliferation and cell cycle arrest in the intestinal epithelium unlike control mice

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

growth/size/body
• in doxycycline-treated adult mice
• however, mice regain weight after withdrawal of doxycycline

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




Genotype
MGI:5051636
cx23
Allelic
Composition
Col1a1tm1(tetO-Tcfap2c)Hsc/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-Tcfap2c)Hsc mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Col1a1tm1(tetO-Tcfap2c)Hsc/Col1a1+ Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+ mice show increased proliferation and induced hepatic steatosis

mortality/aging
• within 6 to 7 days of doxycycline treatment

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

liver/biliary system
• after doxycycline treatment
• after doxycycline treatment
• after doxycycline treatment
• after doxycycline treatment, hepatocytes exhibit abnormally bright mitochondria and increased mitophagy compared to in cells from control mice
• after doxycycline treatment, hepatocytes exhibit abnormally bright mitochondria
• after doxycycline treatment, mice exhibit microvesicular steatosis unlike control mice
• after doxycycline treatment

digestive/alimentary system
• after doxycycline treatment, the proliferative zone is expanded to cover crypt and villus compared to in control mice
• 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
• after doxycycline treatment
• 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
• after doxycycline treatment, mice exhibit pancreatic injury unlike control mice

behavior/neurological
• after doxycycline treatment

growth/size/body
• after doxycycline treatment

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

cellular
• after doxycycline treatment, hepatocytes exhibit abnormally bright mitochondria
• after doxycycline treatment
• after doxycycline treatment, the proliferative zone is expanded to cover crypt and villus compared to in control mice
• after doxycycline treatment




Genotype
MGI:5304756
cx24
Allelic
Composition
Col1a1tm1(tetO-RNAi:Rps19)Karl/Col1a1tm1(tetO-RNAi:Rps19)Karl
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-RNAi:Rps19)Karl mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mice die within 2 months following doxycycline treatment

hematopoietic system
• decrease in the frequency of bipotential megakaryocytic-erythroid cells and preGM/GMP progenitor cells at 7 weeks after doxycycline treatment
• by 10 days after doxycycline treatment
• absolute numbers of all hematopoietic stem and progenitor cells are reduced at 7 weeks after doxycycline treatment
• seven weeks after doxycycline treatment
• decrease in the frequency or proerythroblasts in the bone marrow by 10 days after doxycycline treatment
• seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• seven weeks after doxycycline treatment
• seven weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• preMegE and preCFU-E/CFU-E progenitors show impaired proliferation and increased apoptosis following doxycycline treatment

growth/size/body
• following doxycycline treatment

digestive/alimentary system
• occasional dilated glands in the large intestine and colon

immune system
• seven weeks after doxycycline treatment
• 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
cx25
Allelic
Composition
Col1a1tm1(tetO-RNAi:Rps19)Karl/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-RNAi:Rps19)Karl mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• unlike homozygous mice, heterozygotes survive at least 3 months following doxycycline treatment

hematopoietic system
• decrease in the frequency of bipotential megakaryocytic-erythroid cells and preGM/GMP progenitor cells at 7 weeks after doxycycline treatment
• by 10 days after doxycycline treatment
• absolute numbers of all hematopoietic stem and progenitor cells are reduced at 7 weeks after doxycycline treatment
• seven weeks after doxycycline treatment
• decrease in the frequency or proerythroblasts in the bone marrow by 10 days after doxycycline treatment
• seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• preMegE and preCFU-E/CFU-E progenitors show impaired proliferation and increased apoptosis following doxycycline treatment

immune system
• two and seven weeks after doxycycline treatment

growth/size/body
• following doxycycline treatment
• less pronounced than in homozygous mice

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




Genotype
MGI:5304758
cx26
Allelic
Composition
Col1a1tm2(tetO-RNAi:Rps19)Karl/Col1a1tm2(tetO-RNAi:Rps19)Karl
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-RNAi:Rps19)Karl mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mice die within 2 months following doxycycline treatment

hematopoietic system
• seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• seven weeks after doxycycline treatment
• seven weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• two weeks after doxycycline treatment

growth/size/body
• following doxycycline treatment

immune system
• seven weeks after doxycycline treatment
• 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
cx27
Allelic
Composition
Col1a1tm2(tetO-RNAi:Rps19)Karl/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-RNAi:Rps19)Karl mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• unlike homozygous mice, heterozygotes survive at least 3 months following doxycycline treatment

hematopoietic system
• seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• seven weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• two weeks after doxycycline treatment

growth/size/body
• following doxycycline treatment
• less pronounced than in homozygous mice

immune system
• 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:3703249
cx28
Allelic
Composition
Col1a1tm2(tetO-Pou5f1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-Pou5f1)Jae mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 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
• after doxycline treatment, dysplastic cells are found in the entire epithelium; cells have structural and cytological dysplasia which mimics adenocarcinoma
• 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
• in doxycycline treated mice, cells in the forestomach show a marked atypia and increased mitotic activity
• pyloric mucosa contains lesions resembling high grade-dysplasia in doxycycline treated mice
• hyperplastic fundic glands are seen in doxycycline treated mice
• 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
• after doxycycline treatment, mice display severe dysplasia and increased proliferation
• cells show atypia and increased mitotic activity throughout the squamous epithelial layer in doxycycline treated mice

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

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

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

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

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

integument
• increased numbers of immature cells in the hair follicles of the skin are seen after 5-10 days of doxycycline
• after 5-10 days of doxycycline treatment, mice show mild to moderate epidermal dysplasia with a decrease in differentiation in dysplastic cells
• in doxycycline treated mice, tumors originating from the outer-root-sheath progenitors and invading the subcutaneous layer are seen

endocrine/exocrine glands
• hyperplastic fundic glands are seen in doxycycline treated mice
• atrophy and absence of CD4, CD8 double positive cells in doxycycline treated mice




Genotype
MGI:4430610
cx29
Allelic
Composition
Col1a1tm3(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae/Col1a1tm3(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm3(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice exhibit no tumors or health problems up to 31 weeks




Genotype
MGI:4822382
cx30
Allelic
Composition
Col1a1tm6(tetO-MSI2)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm6(tetO-MSI2)Jae mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 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
• 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
• 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
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1
• 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
• 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
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1
• at 6 weeks, but not 16 weeks, in wild-type mice reconstituted with bone marrow and treated with doxycyline
• at 6 and 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline
• at 6 and 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline
• at 6 weeks, but not 16 weeks, in wild-type mice reconstituted with bone marrow and treated with doxycyline
• 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
• at 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline
• at 6 and 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

liver/biliary system
• 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
• 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
• 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
• 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
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1
• 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
• at 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline
• at 6 and 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

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




Genotype
MGI:4999980
cx31
Allelic
Composition
Col1a1tm1(tetO-GFP/RNAi:luc)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-GFP/RNAi:luc)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• doxycycline-treated mice are normal




Genotype
MGI:4999985
cx32
Allelic
Composition
Col1a1tm3(tetO-GFP/RNAi:Apc)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm3(tetO-GFP/RNAi:Apc)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• doxycycline-treated mice with lymphoma exhibit median survival of 7.4 months

skeleton
• 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
• 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
• 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
• in mice treated with doxycycline beyond 20 weeks
• however, reactivation after 4 weeks by doxycycline withdrawal prevents hair loss
• in mice treated with doxycycline beyond 20 weeks

homeostasis/metabolism
• 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
• 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
• mice transiently treated with doxycycline between E8.5 and E12.5 exhibit severely stunted hind- and forelimb development compared with wild-type mice
• 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
• in mice treated with doxycycline 1 to 2 days prior to birth
• reactivation after 4 weeks of doxycycline treatment does not rescue stunted snout
• runting in mice treated with doxycycline 1 to 2 days prior to birth
• in mice treated with doxycycline 1 to 2 days prior to birth
• at E14.5 and E18.5 in mice treated with doxycycline at E8.5

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

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

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

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




Genotype
MGI:4999987
cx33
Allelic
Composition
Col1a1tm4(tetO-GFP/RNAi:Apc)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm4(tetO-GFP/RNAi:Apc)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• doxycycline-treated mice with lymphoma exhibit median survival or 5.3 months

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

integument
• 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
• in mice treated with doxycycline beyond 20 weeks
• however, reactivation after 4 weeks of doxycycline prevents hair loss
• in mice treated with doxycycline beyond 20 weeks

craniofacial
• 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
• in mice treated with doxycycline 1 to 2 days prior to birth
• reactivation after 4 weeks of doxycycline treatment does not rescue stunted snout
• runting in mice treated with doxycycline 1 to 2 days prior to birth
• in mice treated with doxycycline 1 to 2 days prior to birth

endocrine/exocrine glands
• in mice treated with doxycycline from 4 to 6 weeks of age

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

hematopoietic system
• 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:5478622
cx34
Allelic
Composition
Col1a1tm1(tetO-Yod1*)Hpl/Col1a1tm1(tetO-Yod1*)Hpl
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-Yod1*)Hpl mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• doxycycline-treated mice exhibit normal T cell distribution in lymphoid organs
• CD8+ T cells from doxycycline-treated mice exhibit enhanced response to immunization with viral infection and improved viral growth control compared with control cells
• 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
• 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
cx35
Allelic
Composition
Col1a1tm1(tetO-EWSR1/ATF1)Yasu/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-EWSR1/ATF1)Yasu mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• after 3 to 10 months of doxycycline-treated mice with median survival of 20 weeks

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

cellular
• 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
cx36
Allelic
Composition
Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda/?
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• in doxycycline-treated neonates

cellular
• in doxycycline-treated neonates




Genotype
MGI:5585616
cx37
Allelic
Composition
Col1a1tm1(tetO-Cyp26b1)Mfra/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-Cyp26b1)Mfra mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mice treated with doxycycline at E8.5 exhibit smaller jugular lymph sac at E 14.5 compared with control mice




Genotype
MGI:5586502
cx38
Allelic
Composition
Col1a1tm3(tetO-Fosl1,-DsRed)Wag/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm3(tetO-Fosl1,-DsRed)Wag mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• periportal with immune infiltrate in doxycycline-treated mice

skeleton
• in doxycycline-treated mice at necropsy

growth/size/body
• in doxycycline-treated mice
• in doxycycline-treated mice at necropsy

behavior/neurological
• in doxycycline-treated mice

homeostasis/metabolism
• sometimes in doxycycline-treated mice at necropsy

hematopoietic system
• in doxycycline-treated mice at necropsy

immune system
• in doxycycline-treated mice at necropsy




Genotype
MGI:5754807
cx39
Allelic
Composition
Col1a1tm1(tetO-U2AF1*S34F)Mjwa/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-U2AF1*S34F)Mjwa mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• 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
cx40
Allelic
Composition
Col1a1tm2(tetO-U2AF1)Mjwa/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-U2AF1)Mjwa mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• transplantation of bone marrow from mutants into lethally-irradiated recipient mice treated with doxycycline does not result in altered hematopoiesis




Genotype
MGI:5911575
cx41
Allelic
Composition
Col1a1tm1(tetO-GFP/RNAi:Rad21)Iaai/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-GFP/RNAi:Rad21)Iaai mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• lineage skewing is seen following prolonged doxycycline exposure (30 days)
• in the splenic parenchyma
• decrease in the Ter119+ cell population
• decrease in the proportion of B cell population (B220+)
• increase in the proportion of myelomonocytic (Cd11b+/Gr1+) and erythroid (CD71+/Ter119+) cells
• increased amount of early erythroid (CD71+/Ter119+) cells in the spleen
• increase in nuclear size in sorted Lineage-/c-Kit+ progenitor cells not associated with an increase of genomic material or instability

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




Genotype
MGI:5911576
cx42
Allelic
Composition
Col1a1tm2(tetO-GFP/RNAi:Smc1a)Iaai/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-GFP/RNAi:Smc1a)Iaai mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• lineage skewing is seen following prolonged doxycycline exposure (30 days)
• in the splenic parenchyma
• decrease in the Ter119+ cell population
• hypercellular bone marrow with erythroid and megakaryocytic hypoplasia and marked myeloid hyperplasia
• in the GFP+ cells in the bone marrow
• in peripheral blood of aged mice
• decrease in the proportion of B cell population (B220+)
• increase in the proportion of myelomonocytic (Cd11b+/Gr1+) and erythroid (CD71+/Ter119+) cells
• increased amount of early erythroid (CD71+/Ter119+) cells in the spleen
• aged mice show marked expansion of myeloid elements (granulocytic > monocytic) in the peripheral blood
• increase in nuclear size in sorted Lineage-/c-Kit+ progenitor cells not associated with an increase of genomic material or instability
• 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

immune system
• aged mice show marked expansion of myeloid elements (granulocytic > monocytic) in the peripheral blood
• in peripheral blood of aged mice
• decrease in the proportion of B cell population (B220+)

growth/size/body

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




Genotype
MGI:5911578
cx43
Allelic
Composition
Col1a1tm3(tetO-GFP/RNAi:Stag2)Iaai/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm3(tetO-GFP/RNAi:Stag2)Iaai mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• lineage skewing is seen following prolonged doxycycline exposure (30 days)
• decrease in the proportion of B cell population (B220+)
• increase in the proportion of myelomonocytic (Cd11b+/Gr1+) and erythroid (CD71+/Ter119+) cells
• increase in nuclear size in sorted Lineage-/c-Kit+ progenitor cells not associated with an increase of genomic material or instability
• decrease in the number of GFP+ cells in the long-term (CD150+) and short-term (CD150-/CD48-) subsets

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




Genotype
MGI:5911579
cx44
Allelic
Composition
Col1a1tm2(tetO-GFP/RNAi:Smc1a)Iaai/Col1a1tm3(tetO-GFP/RNAi:Stag2)Iaai
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-GFP/RNAi:Smc1a)Iaai mutation (0 available); any Col1a1 mutation (163 available)
Col1a1tm3(tetO-GFP/RNAi:Stag2)Iaai mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• lineage skewing is seen following short term doxycycline exposure
• develops over time
• develops over time
• decrease in the proportion of B cell population (B220+) develops over time
• disrupted morphology
• following short term doxycycline exposure

immune system
• develops over time
• decrease in the proportion of B cell population (B220+) develops over time
• disrupted morphology
• following short term doxycycline exposure

growth/size/body
• following short term doxycycline exposure




Genotype
MGI:5316663
cx45
Allelic
Composition
Col1a1tm1(tetO-YAP1*)Fcam/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-YAP1*)Fcam mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice become ill and must be euthanized 4-6 days after doxycycline treatment

digestive/alimentary system
• 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
• 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
• in doxycycline-treated mice
• severe dysplasia in doxycycline-treated mice
• Paneth cells are absent 5 days after doxycycline treatment
• however, the absence of Paneth cells is reversed by doxycycline-withdrawal

endocrine/exocrine glands
• in doxycycline-treated mice
• Paneth cells are absent 5 days after doxycycline treatment
• however, the absence of Paneth cells is reversed by doxycycline-withdrawal
• in doxycycline-treated mice
• ductal metaplasia of pancreatic acinar cells in doxycycline-treated mice

cellular
• 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
• 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
• in the epidermis of doxycycline-treated mice

homeostasis/metabolism
• absent in the small intestine 5 days after doxycycline treatment

integument
• in doxycycline-treated mice

growth/size/body
• in doxycycline-treated mice




Genotype
MGI:5430595
cx46
Allelic
Composition
Col1a1tm1(tetO-Yap1*)Lrsn/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-Yap1*)Lrsn mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die 10 days after treatment with doxycycline




Genotype
MGI:5474007
cx47
Allelic
Composition
Col1a1tm2(tetO-CTNNB1*)Hoch/Col1a1tm2(tetO-CTNNB1*)Hoch
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-CTNNB1*)Hoch mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• suppressed cellular differentiation toward goblet cells
• after doxycycline treatment of adults
• number of intestinal stem cells is increased
• decreased cell division in colonic cells
• crypt fission and budding is normalized after treatment with notch inhibitors
• crypt fission is often observed in the large intestine
• crypt fission is often observed in the small intestine

endocrine/exocrine glands
• crypt fission and budding is normalized after treatment with notch inhibitors
• crypt fission is often observed in the large intestine
• crypt fission is often observed in the small intestine

cellular
• suppressed cellular differentiation toward goblet cells




Genotype
MGI:5313420
cx48
Allelic
Composition
ApcMin/Apc+
Col1a1tm10(tetO-Dnmt3b_i3)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (12 available); any Apc mutation (158 available)
Col1a1tm10(tetO-Dnmt3b_i3)Jae mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• doxycycline-treated mice develop intestinal adenomas at the same rate as in Apcmin heterozygotes




Genotype
MGI:5313423
cx49
Allelic
Composition
ApcMin/Apc+
Col1a1tm12(tetO-Dnmt3a_i1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (12 available); any Apc mutation (158 available)
Col1a1tm12(tetO-Dnmt3a_i1)Jae mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• doxycycline-treated mice develop intestinal adenomas at the same rate as in Apcmin heterozygotes




Genotype
MGI:5313419
cx50
Allelic
Composition
ApcMin/Apc+
Col1a1tm9(tetO-Dnmt3b_i1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (12 available); any Apc mutation (158 available)
Col1a1tm9(tetO-Dnmt3b_i1)Jae mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apcmin heterozygotes
• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apcmin heterozygotes
• doxycycline-treated mice exhibit increased size of microadenomas compared with Apcmin heterozygotes

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




Genotype
MGI:5437856
cx51
Allelic
Composition
Col1a1tm1(tetO-Deptor)Dmsa/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-Deptor)Dmsa mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• doxycycline treated mice gain more weight on a high fat diet; not caused by a difference in food intake or locomotion
• in doxycycline treated mice on a high fat diet
• MEFs treated with doxycycline and differentiated in adipocytes show increased triglyceride accumulation

adipose tissue
• in doxycycline treated mice on a high fat diet

liver/biliary system
• in doxycycline treated mice on a high fat diet
• in doxycycline treated mice on a high fat diet

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




Genotype
MGI:5469373
cx52
Allelic
Composition
Col1a1tm1(tetO-CTNNB1)Tcd/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-CTNNB1)Tcd mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• doxycycline-treated mice exhibit normal villus compartment
• 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
• upon withdrawal of doxycycline
• increased in the crypt compartment of doxycycline-treated mice
• doxycycline-treated mice exhibit partially altered intestinal differentiation compared with control mice
• enlarged crypts in doxycycline-treated mice
• however, withdrawal of doxycycline leads to a rapid regression of the crypt compartment

growth/size/body
• in docycycline-treated mice

endocrine/exocrine glands
• enlarged crypts in doxycycline-treated mice
• however, withdrawal of doxycycline leads to a rapid regression of the crypt compartment

cellular
• 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
• upon withdrawal of doxycycline
• increased in the crypt compartment of doxycycline-treated mice




Genotype
MGI:5313421
cx53
Allelic
Composition
ApcMin/Apc+
Col1a1tm11(tetO-Dnmt3b_i6)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (12 available); any Apc mutation (158 available)
Col1a1tm11(tetO-Dnmt3b_i6)Jae mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• doxycycline-treated mice develop intestinal adenomas at the same rate as in Apcmin heterozygotes




Genotype
MGI:6446222
cx54
Allelic
Composition
Btnl1tm1(KOMP)Mbp/Btnl1tm1(KOMP)Mbp
Gt(ROSA)26Sortm1(rtTA*M2)Jae/0
Tg(tetO-Btnl1)#Ahay/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Btnl1tm1(KOMP)Mbp mutation (2 available); any Btnl1 mutation (30 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Tg(tetO-Btnl1)#Ahay mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• 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
• 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
cx55
Allelic
Composition
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-LIN28B)Gqda mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• following doxycycline treatment mice gain less weight when fed a high fat diet compared to wild-type mice

homeostasis/metabolism
• following doxycycline treatment mice gain less weight when fed a high fat diet compared to wild-type mice
• following doxycycline treatment average fasting glucose is less than 50 mg/dL
• following doxycycline treatment on a normal or high fat diet
• following doxycycline treatment




Genotype
MGI:5294615
cx56
Allelic
Composition
Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• following doxycycline treatment
• following doxycycline treatment

homeostasis/metabolism
• in the fed state following doxycycline treatment
• during a glucose tolerance test in doxycycline treated mice
• however, no difference in insulin sensitivity is detected following doxycycline treatment
• following doxycycline treatment on a normal or high fat diet




Genotype
MGI:5294616
cx57
Allelic
Composition
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-LIN28B)Gqda mutation (1 available); any Col1a1 mutation (163 available)
Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• following doxycycline treatment responses in a glucose tolerance test are similar to controls




Genotype
MGI:5000009
cx58
Allelic
Composition
Col1a1tm10(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(CMV-rtTA)4Bjd/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * NMRI
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm10(tetO*-RFP/RNAi:Rpa3)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Tg(CMV-rtTA)4Bjd mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mice treated with doxycycline between 5 and 10 weeks of age die prematurely

growth/size/body
• in doxycycline-treated mice




Genotype
MGI:5000014
cx59
Allelic
Composition
Col1a1tm11(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(CMV-rtTA)4Bjd/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * NMRI
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm11(tetO*-RFP/RNAi:Rpa3)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Tg(CMV-rtTA)4Bjd mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mice treated with doxycycline between 5 and 10 weeks of age die prematurely

growth/size/body
• in doxycycline-treated mice




Genotype
MGI:5000006
cx60
Allelic
Composition
Col1a1tm8(tetO-GFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(CMV-rtTA)4Bjd/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * NMRI
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm8(tetO-GFP/RNAi:Rpa3)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Tg(CMV-rtTA)4Bjd mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• half of mice treated with doxycycline between 5 and 10 weeks of age die prematurely

growth/size/body
• in doxycycline-treated mice

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




Genotype
MGI:5698051
cx61
Allelic
Composition
Col1a1tm1(tetO-Stat1)Biat/Col1a1tm1(tetO-Stat1)Biat
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Stat1tm1Dlv/Stat1tm1Dlv
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-Stat1)Biat mutation (1 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (992 available)
Stat1tm1Dlv mutation (6 available); any Stat1 mutation (74 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 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
• 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





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last database update
10/29/2024
MGI 6.24
The Jackson Laboratory