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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy
targeted mutation 1, Andras Nagy
MGI:3583817
Summary 30 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Rbpjtm1Hon/Rbpjtm1Hon
Tg(tetO-cre)1Jaw/0
involves: 129 * C57BL/6 MGI:4418250
cn2
Col1a1tm5(tetO-Jun/Fos)Wag/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Alb1-cre)7Gsc/0
involves: 129 * C57BL/6 * FVB/N MGI:5586561
cn3
Col1a1tm1(tetO-Fos)Wag/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Alb1-cre)7Gsc/0
involves: 129 * C57BL/6 * FVB/N MGI:5586562
cn4
Ctnnb1tm2Kem/Ctnnb1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Col2a1-cre)1Bhr/0
Tg(tetO-Vegfa)90Ala/0
involves: 129 * C57BL/6 * FVB/N * ICR * SJL MGI:4429127
cn5
Angpt1tm1.1Seq/Angpt1tm1.1Seq
Angpt2tm1c(KOMP)Seq/Angpt2tm1c(KOMP)Seq
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/?
Tg(tetO-cre)1Jaw/0
involves: 129 * C57BL/6NCr MGI:5613965
cn6
Tektm1.1Vlcg/Tektm1.1Vlcg
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/?
Tg(tetO-cre)1Jaw/0
involves: 129 * C57BL/6NCr MGI:5613966
cn7
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras*G12D)#Rdp/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N MGI:5648533
cn8
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras*G12D)#Rdp/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S/Sv * 129X1/SvJ * C57BL/6 * FVB/N MGI:5648534
cn9
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Wt1tm2(cre/ERT2)Wtp/Wt1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:5638793
cn10
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Wt1tm2(cre/ERT2)Wtp/Wt1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:5638880
cn11
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1+
Foxd1tm1(GFP/cre)Amc/Foxd1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:5638869
cn12
Col1a1tm1(tetO-YAP1*)Fcam/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(KRT14-cre)1Amc/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA MGI:5316468
cn13
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Six2-EGFP/cre)1Amc/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CD-1 MGI:5638867
cn14
Col1a1tm1(tetO-YAP1*)Fcam/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2 MGI:5705651
cn15
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Cdh16-cre)91Igr/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * ICR MGI:5638874
cn16
Bmp4tm2(tetO-Bmp4,lacZ)Jfm/?
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/?
Tg(Mef2c-cre)2Blk/?
involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ MGI:4941612
cn17
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Sox9tm3(cre)Crm/Sox9+
Tg(tetO-Vegfa)1Kesh/0
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ MGI:3840959
cn18
Gt(ROSA)26Sortm1(tetO-Sox9)Msan/Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy
Shhtm1(EGFP/cre)Cjt/Shh+
involves: 129S1/Sv * 129X1/SvJ MGI:5557985
cn19
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Tg(tetO-Xbp1_is)#Pesch/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA * FVB MGI:6376140
cn20
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras*G12D)#Rdp/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N MGI:5648532
cn21
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Col2a1-cre)1Bhr/0
Tg(tetO-Vegfa)90Ala/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N * SJL MGI:4429125
cn22
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras2)12Hev/0
Trp53tm1Tyj/Trp53+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N MGI:5569005
cn23
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras2)12Hev/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N MGI:5569002
cn24
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Prrx1-cre)1Cjt/0
Tg(tetO-Gata6)1Abl/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL/J MGI:5550092
cn25
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Nphs2-cre)1Seq/0
Tg(tetO-Vegfa)90Ala/0
involves: 129S1/Sv * 129X1/SvJ * FVB/N * ICR MGI:3587023
cn26
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(CAG-cre)1Nagy/0
Tg(tetO-Vegfa)90Ala/0
involves: 129S1/Sv * 129X1/SvJ * FVB/N * ICR MGI:3587021
cn27
Bmp4tm2(tetO-Bmp4,lacZ)Jfm/Bmp4+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
H2az2Tg(Wnt1-cre)11Rth/H2az2+
involves: 129/Sv * C57BL/6J * CBA/J MGI:5312862
cn28
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptentm1Rdp/Ptentm1Rdp
Tg(tetO-BRAF*V600E)29Lc/0
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129/Sv * C57BL/6J * FVB * SJL MGI:5700641
cn29
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Nes-cre)1Kln/0
Tg(tetO-Vegfa)90Ala/0
mixed MGI:3587022
cx30
Col4a3tm1Jhm/Col4a3tm1Jhm
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(tetO-COL4A3/Col4a3)#aJhm/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:5559181


Genotype
MGI:4418250
cn1
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Rbpjtm1Hon/Rbpjtm1Hon
Tg(tetO-cre)1Jaw/0
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Rbpjtm1Hon mutation (2 available); any Rbpj mutation (193 available)
Tg(tetO-cre)1Jaw mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• doxycycline-treated mice die shortly after birth

respiratory system
• at E18.5, myofibroblasts in the lungs of doxycycline-treated mice exhibit reduced differentiation, as determined by sma+ expression, compared to in wild-type mice




Genotype
MGI:5586561
cn2
Allelic
Composition
Col1a1tm5(tetO-Jun/Fos)Wag/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Alb1-cre)7Gsc/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm5(tetO-Jun/Fos)Wag mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Alb1-cre)7Gsc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• doxycycline-treated mice develop lethal liver dysplasia

liver/biliary system
• doxycycline-treated mice develop lethal liver dysplasia




Genotype
MGI:5586562
cn3
Allelic
Composition
Col1a1tm1(tetO-Fos)Wag/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Alb1-cre)7Gsc/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-Fos)Wag mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Alb1-cre)7Gsc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• doxycycline-treated mice develop lethal liver dysplasia

liver/biliary system
• doxycycline-treated mice develop lethal liver dysplasia




Genotype
MGI:4429127
cn4
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Col2a1-cre)1Bhr/0
Tg(tetO-Vegfa)90Ala/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N * ICR * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (49 available)
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Col2a1-cre)1Bhr mutation (3 available)
Tg(tetO-Vegfa)90Ala mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• local bone and marrow tissue in doxycycline-treat mice are replaced with massively enlarged vascular structures (hemangiomas) unlike in wild-type mice

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




Genotype
MGI:5613965
cn5
Allelic
Composition
Angpt1tm1.1Seq/Angpt1tm1.1Seq
Angpt2tm1c(KOMP)Seq/Angpt2tm1c(KOMP)Seq
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/?
Tg(tetO-cre)1Jaw/0
Genetic
Background
involves: 129 * C57BL/6NCr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Angpt1tm1.1Seq mutation (0 available); any Angpt1 mutation (35 available)
Angpt2tm1c(KOMP)Seq mutation (0 available); any Angpt2 mutation (46 available)
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(tetO-cre)1Jaw mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• capillary loops extend into the cornea

vision/eye
• in mice exposed to deoxycycline treatment at E16.5
• lymphatic vasculature develops in the corneal limbus
• capillary loops extend into the cornea
• increased anterior chamber depth
• eyes begin to protrude by 21 to 28 days of age
• difficulty closing eyelids by 8 weeks of age
• reduced thickness of retinal cell layer
• becoming worse toward periphery
• in mice exposed to deoxycycline treatment at E16.5
• severely impaired vision

immune system
• lymphatic vessels are sparse in the dermis of the ear
• abnormal branching of lymphatic vessels




Genotype
MGI:5613966
cn6
Allelic
Composition
Tektm1.1Vlcg/Tektm1.1Vlcg
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/?
Tg(tetO-cre)1Jaw/0
Genetic
Background
involves: 129 * C57BL/6NCr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tektm1.1Vlcg mutation (0 available); any Tek mutation (92 available)
Tg(tetO-cre)1Jaw mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• in mice exposed to deoxycycline treatment at E16.5
• increased anterior chamber depth
• eyes begin to protrude by 21 to 28 days of age in mice exposed to deoxycycline treatment at E16.5
• difficulty closing eyelids by 8 weeks of age




Genotype
MGI:5648533
cn7
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras*G12D)#Rdp/0
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Tg(tetO-Kras*G12D)#Rdp mutation (0 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) between 11 and 25 weeks of age following doxycycline treatment at 3 weeks of age
• tumors exhibit features of human PDAC, including glandular tumor structures, exuberant stroma, local invasion into surrounding structures such as the duodenum, and distant metastases to the liver and lung
• mice show rapid tumor regression staring 48 hours and peaking at 72 hours following doxycycline withdrawal, with a reduction in tumor mass of about 50% after 1 week of doxycycline withdrawal; tumor regression is accompanied by decreased tumor cell proliferation and increased apoptosis
• withdrawal of doxycycline results in decreased glucose uptake and lactate production by cells in vitro

endocrine/exocrine glands
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) between 11 and 25 weeks of age following doxycycline treatment at 3 weeks of age
• tumors exhibit features of human PDAC, including glandular tumor structures, exuberant stroma, local invasion into surrounding structures such as the duodenum, and distant metastases to the liver and lung
• mice show rapid tumor regression staring 48 hours and peaking at 72 hours following doxycycline withdrawal, with a reduction in tumor mass of about 50% after 1 week of doxycycline withdrawal; tumor regression is accompanied by decreased tumor cell proliferation and increased apoptosis
• withdrawal of doxycycline results in decreased glucose uptake and lactate production by cells in vitro

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:186194




Genotype
MGI:5648534
cn8
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras*G12D)#Rdp/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S/Sv * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Tg(tetO-Kras*G12D)#Rdp mutation (0 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) at a median age of 7.9 weeks following doxycycline treatment at 3 weeks of age

endocrine/exocrine glands
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) at a median age of 7.9 weeks following doxycycline treatment at 3 weeks of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:186194




Genotype
MGI:5638793
cn9
Allelic
Composition
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Wt1tm2(cre/ERT2)Wtp/Wt1+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6
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,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Wt1tm2(cre/ERT2)Wtp mutation (1 available); any Wt1 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• all mice develop kidney tumors within the first 2 weeks of life following doxycycline (Dox) induction during embryonic development at E0, E14.5 or E18.5
• tumors resemble Wilms tumor
• mice treated with doxycycline at P10 do not develop tumors

renal/urinary system
• mice treated with doxycycline at P10 develop cystic kidneys
• all mice develop kidney tumors within the first 2 weeks of life following doxycycline (Dox) induction during embryonic development at E0, E14.5 or E18.5
• tumors resemble Wilms tumor
• mice treated with doxycycline at P10 do not develop tumors
• doxycycline induced mice exhibit persistent proliferation of cap mesenchyme cells in adults
• however, cap mesenchyme cells within tumors retain a differentiation capacity that recapitulates normal kidney development
• timing of kidney development is prolonged in doxycycline induced mice, with sustaining proliferation of the cap mesenchyme cells into adulthood

growth/size/body
• mice treated with doxycycline at P10 develop cystic kidneys

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
nephroblastoma DOID:2154 OMIM:194070
J:211179




Genotype
MGI:5638880
cn10
Allelic
Composition
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Wt1tm2(cre/ERT2)Wtp/Wt1+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6
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,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Wt1tm2(cre/ERT2)Wtp mutation (1 available); any Wt1 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• small kidney in mice induced with doxycycline from E14.5 until the end of the experiment
• however, cap mesenchyme differentiates normally in doxycycline induced mutants




Genotype
MGI:5638869
cn11
Allelic
Composition
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1+
Foxd1tm1(GFP/cre)Amc/Foxd1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm2(tetO-LIN28B)Gqda mutation (1 available); any Col1a1 mutation (163 available)
Foxd1tm1(GFP/cre)Amc mutation (1 available); any Foxd1 mutation (13 available)
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• mice develop hydronephrosis following doxycycline induction

neoplasm
N
• mice do not develop renal tumors following doxycycline induction




Genotype
MGI:5316468
cn12
Allelic
Composition
Col1a1tm1(tetO-YAP1*)Fcam/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(KRT14-cre)1Amc/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA
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,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(KRT14-cre)1Amc mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• skin grafts on nude mice treated with doxycycline exhibit stunted hair growth unlike control grafts
• doxycycline-treated mice exhibit multi-layered epithelium unlike control mice
• skin grafts on nude mice treated with doxycycline exhibit hyperkeratosis unlike control grafts
• skin grafts on nude mice treated with doxycycline exhibit hyperkeratosis unlike control grafts
• 8 days after doxycycline treatment
• 8 days after doxycycline treatment
• skin from doxycycline-treated mice exhibit a greater than 5-fold increase in the number of colony-forming cells compared with skin from control mice
• in nude mice receiving skin grafts and treated with doxycycline

craniofacial
• thickened and dysplastic in doxycycline-treated mice

neoplasm
• in nude mice receiving skin grafts and treated with doxycycline

cellular
• doxycycline-treated mice exhibit increased cell proliferation of basal cells and an extension of the proliferative domain into the suprabasal layers of back skin compared with control mice

digestive/alimentary system
• thickened and dysplastic in doxycycline-treated mice

growth/size/body
• thickened and dysplastic in doxycycline-treated mice




Genotype
MGI:5638867
cn13
Allelic
Composition
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Six2-EGFP/cre)1Amc/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * 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,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Six2-EGFP/cre)1Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• mice develop cystic kidneys when transgene expression is induced with doxycycline early in embryonic development or in adult mice

neoplasm
N
• mice do not develop renal tumors following doxycycline induction

growth/size/body
• mice develop cystic kidneys when transgene expression is induced with doxycycline early in embryonic development or in adult mice




Genotype
MGI:5705651
cn14
Allelic
Composition
Col1a1tm1(tetO-YAP1*)Fcam/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2
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,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 4 of 11 mice administered doxycycline at 3 months of age develop prostate tumors with age
• tumors include adenocarcinomas, sarcomatoid carcinomas (epithelial-mesenchymal transition-like epithelial tumor), and stromal-type tumors

endocrine/exocrine glands
• 4 of 11 mice administered doxycycline at 3 months of age develop prostate tumors with age
• tumors include adenocarcinomas, sarcomatoid carcinomas (epithelial-mesenchymal transition-like epithelial tumor), and stromal-type tumors

reproductive system
• 4 of 11 mice administered doxycycline at 3 months of age develop prostate tumors with age
• tumors include adenocarcinomas, sarcomatoid carcinomas (epithelial-mesenchymal transition-like epithelial tumor), and stromal-type tumors




Genotype
MGI:5638874
cn15
Allelic
Composition
Col1a1tm2(tetO-LIN28B)Gqda/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Cdh16-cre)91Igr/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * ICR
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,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Cdh16-cre)91Igr mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
N
• no kidney pathology is seen in mice induced with doxycycline




Genotype
MGI:4941612
cn16
Allelic
Composition
Bmp4tm2(tetO-Bmp4,lacZ)Jfm/?
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/?
Tg(Mef2c-cre)2Blk/?
Genetic
Background
involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmp4tm2(tetO-Bmp4,lacZ)Jfm mutation (0 available); any Bmp4 mutation (23 available)
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Mef2c-cre)2Blk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• in the right ventricle and out flow tract
• thickening of the myocardium
• thickening of the myocardium

muscle
• in the right ventricle and out flow tract




Genotype
MGI:3840959
cn17
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Sox9tm3(cre)Crm/Sox9+
Tg(tetO-Vegfa)1Kesh/0
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Sox9tm3(cre)Crm mutation (1 available); any Sox9 mutation (33 available)
Tg(tetO-Vegfa)1Kesh mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• the vascular network of the limbs is denser and more complex
• metacarpal centers are enriched for thicker vessels originating from the axial artery
• metacarpal centers are wider and split into a denser and more complex network of small capillaries in the interdigital areas
• however, formation of avascular areas is not affected




Genotype
MGI:5557985
cn18
Allelic
Composition
Gt(ROSA)26Sortm1(tetO-Sox9)Msan/Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy
Shhtm1(EGFP/cre)Cjt/Shh+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Gt(ROSA)26Sortm1(tetO-Sox9)Msan mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Shhtm1(EGFP/cre)Cjt mutation (1 available); any Shh mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• decrease in airway spaces at E18.5
• develop large, cyst-like structures at the distal epithelial branch tips
• cystic buds appear to collapse by E18.5
• noticeable by E14.5 and more significant by E16.5

growth/size/body
• develop large, cyst-like structures at the distal epithelial branch tips
• cystic buds appear to collapse by E18.5




Genotype
MGI:6376140
cn19
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Tg(tetO-Xbp1_is)#Pesch/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
Tg(tetO-Xbp1_is)#Pesch mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• doxycycline (Dox)-treated mice show a gradual reduction in the volume of adipose tissue
• when mice are taken off the Dox-containing diet, the fat tissue volume increases

homeostasis/metabolism
• increase in serum free fatty acids in the fed state after 72 hours of induction with Dox
• however, Dox-treated mice maintain the same rate of fatty acid and cholesterol synthesis as controls in a biochemical assay for de novo lipid synthesis
• mice fed a doxycycline (Dox)-containing diet show a higher respiratory exchange ratio than wild-type mice during the dark phase
• mice exhibit a reduction in hepatic glucose release when exposed to Dox for 48 hours
• metabolic cage studies indicate higher glucose utilization in Dox-treated mice
• a 6-hour fast causes severe hypoglycemia within 48 hours after induction with Dox
• serum glucose levels start to decrease by 72 hours after induction with Dox under fed conditions
• administration of a PPAR-alpha agonist exacerbates the hypoglycemia in Dox-treated mice
• fed insulin levels start to decrease upon induction with Dox and are significantly lower by 72 hours of induction
• 96 hours after Dox-induction, fasted insulin levels are lower
• hepatic glycogen is severely depleted after 48 hours of induction with Dox
• livers of Dox-treated mice show a faster response to insulin exposure and isolated hepatocytes induced with Dox show an enhanced insulin response indicating hepatic insulin sensitivity
• hepatic triglyceride content is increased in Dox-treated mice
• a 6-hour fast increases liver triglyceride content acutely within 24 hours of Dox exposure
• the fasting effects of adipocyte lipolysis on hepatic triglyceride content are exacerbated in Dox-treated mice compared to wild-type mice

liver/biliary system
• liver mass is increased 1.7-fold within 48 hours of induction with Dox
• Dox-treated mice show reduced dry mass content per wet liver
• increase in total liver protein in Dox-treated mice
• hepatic glycogen is severely depleted after 48 hours of induction with Dox
• hepatic triglyceride content is increased in Dox-treated mice
• a 6-hour fast increases liver triglyceride content acutely within 24 hours of Dox exposure
• Dox-treated mice show an increase in hepatic lipid levels
• when mice are taken off the Dox-containing diet, the liver steatosis decreases rapidly




Genotype
MGI:5648532
cn20
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras*G12D)#Rdp/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Tg(tetO-Kras*G12D)#Rdp mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• infrequently, mice exhibit occurrence of invasive pancreatic ductal adenocarcinoma after long latency (35-70 weeks) following doxycline treatment
• mice develop PanIN lesions within 2 weeks of doxycycline induction
• mice develop acinar-to-ductal metaplasia within 2 weeks of doxycycline induction

neoplasm
• infrequently, mice exhibit occurrence of invasive pancreatic ductal adenocarcinoma after long latency (35-70 weeks) following doxycline treatment
• mice develop PanIN lesions within 2 weeks of doxycycline induction




Genotype
MGI:4429125
cn21
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Col2a1-cre)1Bhr/0
Tg(tetO-Vegfa)90Ala/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Col2a1-cre)1Bhr mutation (3 available)
Tg(tetO-Vegfa)90Ala mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• doxycycline-treated mice exhibit a increase metaphyseal microvascular density compared to in wild-type mice
• following doxycycline treatment for the first 2 weeks of life, growing long bones are abnormal in shape and morphology with abundant stromal cells and blood vessels surrounding numerous trabeculae unlike in wild-type mice
• adult mice treated with doxycycline for 14 days exhibit disrupted bone architecture with abundant peritrabecular mesenchymal stromal cells in the metaphyseal and epiphyseal regions compared with wild-type mice
• adult mice treated with doxycycline for 14 days exhibit lamellar cortical bone is replaced with trabecular-like porous bone structure with abundant intercalating mesenchymal tissue components and osteoclast-rich remodelling units unlike in wild-type mice
• doxycycline-treated mice exhibit reduced osteoclast numbers in regions of excessive bone and vascularization compared with wild-type mice
• however, osteoclast coverage and bone remodeling are normal in the cortical regions of bone following doxycycline treatment
• in doxycycline-treated mice, bone marrow blood vessels exhibit hemangioma-like morphology and are filled with erythrocytes unlike in wild-type mice
• in doxycycline-treated mice, hematopoietic bone marrow is replaced with new bone, marrow fibrosis, and aberrant blood vessels displaying paucity of myeloid cells unlike in wild-type mice
• doxycycline-treated mice exhibit bone marrow fibrosis unlike in wild-type mice
• adult mice treated with doxycycline for 14 days exhibit a 70% increase in trabecular density compared with wild-type mice
• adult mice treated with doxycycline for 14 days exhibit increased metaphyseal trabecular bone mass compared with wild-type mice
• at E16.5, doxycycline-treated mice exhibit increased cell proliferation in the perichondrium/periosteum and throughout the primary ossification center compared with wild-type mice
• adult mice treated with doxycycline exhibit increased proliferation of the mesenchymal cells in the metaphysis, epiphysis, and periosteum compared with wild-type mice
• in doxycycline-treated mice as determined by marker expression
• doxycycline-treated mice exhibit a increase in growth plate mineralization compared to in wild-type mice
• doxycycline-treated mice exhibit a mild decrease in growth plate thickness compared to in wild-type mice
• increased following doxycycline treatment
• doxycycline-treated mice exhibit reduced bone resorption in the diaphyses and metaphysis compared with wild-type mice
• however, osteoclast coverage and bone remodeling are normal in the cortical regions of bone following doxycycline treatment

hematopoietic system
• doxycycline-treated mice exhibit an increase in CFU-Cs (colony-forming units in culture) in the peripheral blood and spleen compared with wild-type mice
• however, bone marrow CFUs of doxycycline-treated mice are normal
• in 25% of doxycycline-treated mice indicating extramedullary hematopoiesis
• as indicated by enlarged spleen size in 25% of doxycycline-treated mice
• in the spleen of doxycycline-treated mice
• the number of megakarypcyte and progenitor cells in the spleens of doxycycline-treated mice is increased compared to in wild-type mice
• small after 2 weeks of doxycycline treatment
• doxycycline-treated mice exhibit reduced osteoclast numbers in regions of excessive bone and vascularization compared with wild-type mice
• however, osteoclast coverage and bone remodeling are normal in the cortical regions of bone following doxycycline treatment
• in the peripheral blood of doxycycline-treated mice

cardiovascular system
• following doxycycline treatment, bone vasculogenesis is increased compared to in wild-type mice
• in doxycycline treated mice, bone marrow blood vessels exhibit hemangioma-like morphology and are filled with erythrocytes unlike in wild-type mice

immune system
• in 25% of doxycycline-treated mice indicating extramedullary hematopoiesis
• doxycycline-treated mice exhibit reduced osteoclast numbers in regions of excessive bone and vascularization compared with wild-type mice
• however, osteoclast coverage and bone remodeling are normal in the cortical regions of bone following doxycycline treatment

cellular
• in doxycycline-treated mice as determined by marker expression

growth/size/body
• in 25% of doxycycline-treated mice indicating extramedullary hematopoiesis




Genotype
MGI:5569005
cn22
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras2)12Hev/0
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Tg(tetO-Kras2)12Hev mutation (1 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die between 8 and 18 weeks after doxycycline (dox) treatment to induce Kras2 expression due to pancreatic ductal adenocarinoma

neoplasm
• mice develop invasive adenocarcinoma between 8 and 18 weeks after dox treatment, with some cases showing hemorrhagic ascites, with admixed poorly differentiated and well-differentiated areas and duodenal invasion
• mice in which dox is removed recover their health and show pancreatic tumor regression resulting in a small pancreatic remnant
• adult mice treated with dox 72 hours prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis develop PanINs, dilated ducts with the presence of intracellular mucins, and extensive fibroinflammatory stroma

homeostasis/metabolism
• adult mice treated with dox for 5 weeks prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis exhibit a small, translucent remnant of pancreatic tissue, without fibrosis or PanIN lesions
• when dox is removed after pancreatitis induction, mice show show normal acini interspersed with dilated ducts and acinar-ductal metaplasia, fibrosis and occasional lipomatosis, but with minimal inflammatory infiltrate, and reduced proliferation

endocrine/exocrine glands
• mice develop invasive adenocarcinoma between 8 and 18 weeks after dox treatment, with some cases showing hemorrhagic ascites, with admixed poorly differentiated and well-differentiated areas and duodenal invasion
• mice in which dox is removed recover their health and show pancreatic tumor regression resulting in a small pancreatic remnant
• adult mice treated with dox 72 hours prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis develop PanINs, dilated ducts with the presence of intracellular mucins, and extensive fibroinflammatory stroma

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




Genotype
MGI:5569002
cn23
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras2)12Hev/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Tg(tetO-Kras2)12Hev mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 1 of 2 mice treated with doxycycline (dox) at 4-6 weeks of age show frank adenocarcinoma by 23 weeks on dox
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein to induce acute pancreatitis show low- and high-grade PanIN lesions interspersed with areas of carcinoma in situ at 5 weeks after induction
• mice treated with doxycycline (dox) at 4-6 weeks of age to induce Kras2 expression begin to show low-grade pancreatic intraepithelial neoplasia (PanIN) beginning at 3 weeks after dox treatment
• mice treated with dox at 4-6 weeks of age show PanIN, surrounded by areas of fibrosis and embedded in the acinar parenchyma after 18 weeks on dox and by 23 weeks, large areas of the pancreatic parenchyma are substituted with PanIN lesions of different grade, with frank adenocarcinoma seen in 1 of 2 mice
• mice kept on dox for 23 weeks show reversion of PanINs when dox is removed for 2 weeks
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein, to induce acute pancreatitis, develop low- and high-grade PanIN lesions at 5 weeks after induction
• mice treated with dox 72 hours prior to induction of pancreatitis also show reversion of PanINs when dox is removed for 2 weeks

homeostasis/metabolism
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein to induce acute pancreatitis show impaired recovery from pancreatitis, showing acinar-ductal metaplasia with progressive accumulation of fibrotic stroma at 1 week after induction, replacement of the whole pancreatic parenchyma with ductal structures and signs of PanINs at 3 weeks after induction, and low- and high-grade PanIN lesions interspersed with areas of carcinoma in situ at 5 weeks after induction compared to adult mice without dox which show completely resolved damage
• mice kept on dox for 5 weeks prior to induction of pancreatitis and then dox removal for 2 weeks show incomplete repair process resulting in a small, fibrotic pancreas with fewer acini; after 5 weeks of dox removal, no PanINs are observed however, the pancreas appears fibrotic and is small

endocrine/exocrine glands
• mice kept on dox for 5 weeks following pancreatitis induction show an increase in apoptotic cells and small pancreas size upon removal of dox
• 1 of 2 mice treated with doxycycline (dox) at 4-6 weeks of age show frank adenocarcinoma by 23 weeks on dox
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein to induce acute pancreatitis show low- and high-grade PanIN lesions interspersed with areas of carcinoma in situ at 5 weeks after induction
• mice treated with doxycycline (dox) at 4-6 weeks of age to induce Kras2 expression begin to show low-grade pancreatic intraepithelial neoplasia (PanIN) beginning at 3 weeks after dox treatment
• mice treated with dox at 4-6 weeks of age show PanIN, surrounded by areas of fibrosis and embedded in the acinar parenchyma after 18 weeks on dox and by 23 weeks, large areas of the pancreatic parenchyma are substituted with PanIN lesions of different grade, with frank adenocarcinoma seen in 1 of 2 mice
• mice kept on dox for 23 weeks show reversion of PanINs when dox is removed for 2 weeks
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein, to induce acute pancreatitis, develop low- and high-grade PanIN lesions at 5 weeks after induction
• mice treated with dox 72 hours prior to induction of pancreatitis also show reversion of PanINs when dox is removed for 2 weeks
• mice treated with dox at 4-6 weeks of age begin to show acinar-ductal metaplasia beginning at 3 weeks after dox treatment




Genotype
MGI:5550092
cn24
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Prrx1-cre)1Cjt/0
Tg(tetO-Gata6)1Abl/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Prrx1-cre)1Cjt mutation (2 available)
Tg(tetO-Gata6)1Abl mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
limbs/digits/tail
• forelimbs and hindlimbs of pups exhibit a reduction in the number of digits following doxycycline administration to dams from E4.5 to E11.5




Genotype
MGI:3587023
cn25
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Nphs2-cre)1Seq/0
Tg(tetO-Vegfa)90Ala/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * FVB/N * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Nphs2-cre)1Seq mutation (0 available)
Tg(tetO-Vegfa)90Ala mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• administration of doxycycline in the drinking water to 4 month old mice and consequent VEGF-A164 expression in podocyte of glomerulus caused proteinuria after 7 days of treatment

renal/urinary system
• administration of doxycycline in the drinking water to 4 month old mice and consequent VEGF-A164 expression in podocyte of glomerulus caused proteinuria after 7 days of treatment




Genotype
MGI:3587021
cn26
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(CAG-cre)1Nagy/0
Tg(tetO-Vegfa)90Ala/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * FVB/N * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(CAG-cre)1Nagy mutation (1 available)
Tg(tetO-Vegfa)90Ala mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused death in 3 out of 8 and moribund appearance in rest of animals after 5 days of treatment
• administration of doxycycline to pregnant dam starting at day E1.5 and consequent VEGF-A164 expression in all embryonic cell caused lethality at E9.5 with no primitive red blood cells in the developing yolk sac and abnormal blood island

homeostasis/metabolism
• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused edema of the face, ears and feet after 2 days of treatment

liver/biliary system
• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused "peliosis-like" liver characterized by an extended blood filed enlarged hepatic sinusoids and a total disruption of the normal liver architecture and blood in the intestine after 5 days of treatment

immune system
• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused a decrease in cellularity and decreased size in thymus after 5 days of treatment
• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused enlarged lymph nodes after 5 days of treatment

hematopoietic system
• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused a decrease in cellularity and decreased size in thymus after 5 days of treatment

integument
• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused erythema of the face, ears and feet after 2 days of treatment

endocrine/exocrine glands
• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused a decrease in cellularity and decreased size in thymus after 5 days of treatment

cardiovascular system
• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused "peliosis-like" liver characterized by an extended blood filed enlarged hepatic sinusoids and a total disruption of the normal liver architecture and blood in the intestine after 5 days of treatment




Genotype
MGI:5312862
cn27
Allelic
Composition
Bmp4tm2(tetO-Bmp4,lacZ)Jfm/Bmp4+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
H2az2Tg(Wnt1-cre)11Rth/H2az2+
Genetic
Background
involves: 129/Sv * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmp4tm2(tetO-Bmp4,lacZ)Jfm mutation (0 available); any Bmp4 mutation (23 available)
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
H2az2Tg(Wnt1-cre)11Rth mutation (2 available); any H2az2 mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial
• following doxycycline treatment at E10.5 a strong reduction in rostral bony elements is seen and multiple translucent areas are seen in the skull bones
• later treatment with doxycycline has less dramatic effects on bone morphology
• enlarged following doxycycline treatment at E12.5
• reduced or absent following doxycycline treatment at E12.5
• following doxycycline treatment at E12.5
• following doxycycline treatment at E12.5
• doxycycline treatment at E11.5 or E10.5 results in a shorter mandible with a more pointed appearance
• doxycycline treatment at E13.5 results in a mandible with a more pointed appearance
• reduced following doxycycline treatment at E13.5
• following doxycycline treatment at E12.5, E11.5 or at E10.5
• doxycycline treatment at E10.5 results in a shorter maxilla with a more pointed appearance
• following doxycycline treatment at E10.5
• following doxycycline treatment at E12.5 in some mice
• following doxycycline treatment at E10.5, E12.5, or E13.5
• shortened face following doxycycline treatment at E10.5
• following doxycycline treatment at E12.5
• enlarged nasal cartilages following doxycycline treatment at E12.5 or E10.5
• following doxycycline treatment at E10.5 the overall shape of the head is more rounded

vision/eye
• following doxycycline treatment at E10.5 the orientation of the eyes is more anterior

respiratory system
• following doxycycline treatment at E12.5 in some mice
• following doxycycline treatment at E10.5, E12.5, or E13.5
• enlarged nasal cartilages following doxycycline treatment at E12.5 or E10.5

digestive/alimentary system
• following doxycycline treatment at E12.5

skeleton
• following doxycycline treatment at E10.5 a strong reduction in rostral bony elements is seen and multiple translucent areas are seen in the skull bones
• later treatment with doxycycline has less dramatic effects on bone morphology
• enlarged following doxycycline treatment at E12.5
• reduced or absent following doxycycline treatment at E12.5
• following doxycycline treatment at E12.5
• following doxycycline treatment at E12.5
• doxycycline treatment at E11.5 or E10.5 results in a shorter mandible with a more pointed appearance
• doxycycline treatment at E13.5 results in a mandible with a more pointed appearance
• reduced following doxycycline treatment at E13.5
• following doxycycline treatment at E12.5, E11.5 or at E10.5
• doxycycline treatment at E10.5 results in a shorter maxilla with a more pointed appearance
• following doxycycline treatment at E10.5
• following doxycycline treatment at E12.5 in some mice
• following doxycycline treatment at E10.5, E12.5, or E13.5
• enlarged nasal cartilages following doxycycline treatment at E12.5 or E10.5

growth/size/body
• following doxycycline treatment at E12.5 in some mice
• following doxycycline treatment at E10.5, E12.5, or E13.5
• shortened face following doxycycline treatment at E10.5
• following doxycycline treatment at E12.5
• enlarged nasal cartilages following doxycycline treatment at E12.5 or E10.5
• following doxycycline treatment at E10.5 the overall shape of the head is more rounded




Genotype
MGI:5700641
cn28
Allelic
Composition
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptentm1Rdp/Ptentm1Rdp
Tg(tetO-BRAF*V600E)29Lc/0
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129/Sv * C57BL/6J * FVB * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1Rdp mutation (6 available); any Cdkn2a mutation (67 available)
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Ptentm1Rdp mutation (0 available); any Pten mutation (88 available)
Tg(tetO-BRAF*V600E)29Lc mutation (0 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen treated mice administered doxycycline in the diet develop melanoma with a median latency of 60 days and with 85% penetrance
• withdrawal of doxycycline leads to rapid tumor regression
• treatment with PLX4720 BRAF inhibitor results in tumor growth inhibition in mutants, however, after continual administration of this inhibitor, mice develop drug resistance




Genotype
MGI:3587022
cn29
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Nes-cre)1Kln/0
Tg(tetO-Vegfa)90Ala/0
Genetic
Background
mixed
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Nes-cre)1Kln mutation (4 available)
Tg(tetO-Vegfa)90Ala mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• administration of doxycycline to pregnant dam starting at day E1.5 and consequent VEGF-A164 expression in neural cell lineage caused vascular abnormalities by E12.5 associated with spinal cord and brain hemorrhages
• administration of doxycycline to pregnant dam starting at day E1.5 and consequent VEGF-A164 expression in neural cell lineage caused vascular abnormalities by E12.5 associated with spinal cord and brain hemorrhages

nervous system
• administration of doxycycline to pregnant dam starting at day E1.5 and consequent VEGF-A164 expression in neural cell lineage caused vascular abnormalities by E12.5 associated with spinal cord and brain hemorrhages
• administration of doxycycline to pregnant dam starting at day E1.5 and consequent VEGF-A164 expression in neural cell lineage caused vascular abnormalities by E12.5 associated with spinal cord and brain hemorrhages

behavior/neurological
N
• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in neural cell lineage did not cause obvious gross behavioral or phenotypic abnormalities in brain after 5 days of treatment




Genotype
MGI:5559181
cx30
Allelic
Composition
Col4a3tm1Jhm/Col4a3tm1Jhm
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(tetO-COL4A3/Col4a3)#aJhm/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col4a3tm1Jhm mutation (1 available); any Col4a3 mutation (62 available)
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(tetO-COL4A3/Col4a3)#aJhm mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
N
• doxycycline-treated mice exhibit normal kidney architecture
• doxycycline-treated mice exhibit some of segmental glomerulus basement membrane thickening observed in Col4a3tm1Jhm homozygotes





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last database update
12/10/2024
MGI 6.24
The Jackson Laboratory