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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gt(ROSA)26Sortm1(cre/ERT)Nat
targeted mutation 1, Jeremy Nathans
MGI:2669525
Summary 34 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sortm1(cre/ERT)Nat B6.129-Gt(ROSA)26Sortm1(cre/Esr1)Nat MGI:2669536
cn2
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sortm3(SS18/EGFP)Mrc involves: 129 * 129S1/Sv * 129X1/SvJ MGI:3843451
cn3
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sortm1(cre/ERT)Nat involves: 129 * C57BL/6 MGI:4443107
cn4
Gt(ROSA)26Sortm5(ASPSCR1/TFE3)Mrc/Gt(ROSA)26Sortm1(cre/ERT)Nat involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:5649275
cn5
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sortm4(EWSR1/ATF1)Mrc involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:5495301
cn6
Telo2tm1Tdl/Telo2tm1.1Tdl
Trp53tm1Tyj/Trp53tm1Tyj
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129 * 129P2/OlaHsd * 129S2/SvPas * C57BL/6J MGI:3819400
cn7
Aurkatm1.1Tvd/Aurkatm1.1Tvd
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sortm1Sor
involves: 129 * 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6J MGI:3836424
cn8
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Lhx2tm1Monu/Lhx2tm1Monu
involves: 129 * 129P2/OlaHsd * C57BL/6 MGI:3772184
cn9
Droshatm1Litt/Droshatm1.1Litt
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129 * 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3806251
cn10
Telo2tm1Tdl/Telo2tm1.1Tdl
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129 * 129P2/OlaHsd * C57BL/6J MGI:3819399
cn11
Aurkatm1.1Tvd/Aurkatm1.1Tvd
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129 * 129P2/OlaHsd * C57BL/6J MGI:3836425
cn12
Acvrl1tm2.1Spo/Acvrl1tm2.1Spo
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129 * 129S1/Sv * 129X1/SvJ MGI:5431572
cn13
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sortm1(cre/ERT)Nat
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129 * 129S2/SvPas * C57BL/6 MGI:4443109
cn14
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sortm1(cre/ERT)Nat
Trp53tm1Tyj/Trp53+
involves: 129 * 129S2/SvPas * C57BL/6 MGI:4443108
cn15
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Ptentm1Hwu/Ptentm1Hwu
involves: 129 * 129S4/SvJae * BALB/c * C57BL/6 MGI:4847601
cn16
Agr2tm1.1Lpkn/Agr2tm1.1Lpkn
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129 * 129S6/SvEvTac * C57BL/6 MGI:4421701
cn17
Atoh1tm3Hzo/Atoh1tm1Hzo
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129 * 129S7/SvEvBrd MGI:4420931
cn18
Atoh1tm3Hzo/Atoh1+
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sortm1(Smo/EYFP)Amc
involves: 129 * 129S7/SvEvBrd * 129X1/SvJ MGI:4420943
cn19
Atoh1tm3Hzo/Atoh1tm1Hzo
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sortm1(Smo/EYFP)Amc
involves: 129 * 129S7/SvEvBrd * 129X1/SvJ MGI:4420935
cn20
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Pdgfratm12Sor/Pdgfra+
involves: 129 * 129/Sv * C57BL/6J * SJL MGI:3838621
cn21
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sortm1(cre/ERT)Nat
Tg(H2-K-BCL2)1Josd/0
involves: 129 * C3H * C57BL/6 MGI:4443111
cn22
Dnaic1tm1.1Leo/Dnaic1tm1.1Leo
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129 * C57BL/6 MGI:4415702
cn23
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Pdgfratm12Sor/Pdgfra+
involves: 129 * C57BL/6 MGI:3838615
cn24
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Tardbptm1.1Pcw/Tardbp+
involves: 129 * C57BL/6 * SJL MGI:4834588
cn25
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Tardbptm1.1Pcw/Tardbptm1.1Pcw
involves: 129 * C57BL/6 * SJL MGI:4834587
cn26
Engtm2.1Hma/Engtm2.1Hma
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ MGI:5775189
cn27
Pkd1tm2Ggg/Pkd1tm2Ggg
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:5587037
cn28
Gpx4tm1.1Qra/Gpx4tm1.1Qra
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * SJL MGI:5425617
cn29
Gdpd5tm1Itl/Gdpd5tm1.1Itl
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129S1/Sv * 129/Sv * 129X1/SvJ * C57BL/6J MGI:5302059
cn30
Fzd4tm1Nat/Fzd4tm2.1Nat
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129S1/Sv * 129X1/SvJ MGI:4948328
cn31
Fzd5tm1Nat/Fzd5tm2Nat
Gt(ROSA)26Sortm1(cre/ERT)Nat/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * SJL MGI:3807225
cn32
Ttc21btm2c(KOMP)Wtsi/Ttc21baln
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6N MGI:5587035
cn33
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Pdgfratm13Sor/Pdgfra+
involves: 129S4/SvJaeSor * C57BL/6 MGI:3838616
cn34
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Ikbkbtm1Lex/Ikbkbtm1Lex
involves: 129S/SvEvBrd MGI:3814551


Genotype
MGI:2669536
hm1
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sortm1(cre/ERT)Nat
Genetic
Background
B6.129-Gt(ROSA)26Sortm1(cre/Esr1)Nat
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype




Genotype
MGI:3843451
cn2
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sortm3(SS18/EGFP)Mrc
Genetic
Background
involves: 129 * 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Gt(ROSA)26Sortm3(SS18/EGFP)Mrc mutation (0 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice treated with tamoxifen exhibit a dosage and frequency dependent lethality dieing by 16 months unlike in mice lacking cre expression

neoplasm
• all mice develop tumors in the juxta-articular region in the limbs with some evidence of calcification
• following tamoxifen treatment, all mice develop tumors in the juxta-articular region in the limbs with some evidence of calcification
• mice develop synovial sarcomas
• following tamoxifen treatment, mice develop synovial sarcomas

Mouse Models of Human Disease
OMIM ID Ref(s)
Sarcoma, Synovial 300813 J:147728




Genotype
MGI:4443107
cn3
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sortm1(cre/ERT)Nat
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• hematopoietic stem and progenitor cells (HSPCs) of mice treated with tamoxifen do not exhibit a selective advantage over cells not expressing the modified cDNA
• the total number of HSPCs is normal in irradiated mice
• following irradiation, the proportion of GFP+ cells in the hematopoietic stem and progenitor cell compartment and myeloid and lymphoid lineages of tamoxifen-treated mice is increased compared to un-irradiated mice
• GFP+ cell accumulation occurs whether mice are treated with tamoxifen 2 or 7 days after irradiation
• however, no competitive advantage is observed when mice are treated with tamoxifen and 5-fluorouracil without DNA damage or over similarly treated Cdkn2atm2.1Rdp cells in irradiated chimera experiments




Genotype
MGI:5649275
cn4
Allelic
Composition
Gt(ROSA)26Sortm5(ASPSCR1/TFE3)Mrc/Gt(ROSA)26Sortm1(cre/ERT)Nat
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Gt(ROSA)26Sortm5(ASPSCR1/TFE3)Mrc mutation (0 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop a tumor within the skull between 3 and 6 months of age; tumors are found primarily in the brain parenchyma, but also in the choroid plexus and orbit
• tumors show characteristic nests of polygonal cells with an open chromatin pattern, surrounded by neatly arcading capillary and larger vascular channels, resembling alveolar soft part sarcoma
• tumors often arise in or near the leptomeninges, along sulci
• some tumors show aggressive invasive growth, with extensions of tumor cells into the cerebellum, cerebrum, and the vessels of the choroid plexus
• mice do not develop tumors in the skeletal muscle
• tumors form in the areas highest in lactate, the cranial vault, express high levels of lactate importers, have abundant mitochondria, metabolize lactate as a metabolic substrate, and respond to exogenous lactate administration with increased cell proliferation and angiogenesis

craniofacial
• mice often exhibit enlargement of the occipital bone from the inner soft tissue expansion

skeleton
• mice often exhibit enlargement of the occipital bone from the inner soft tissue expansion

Mouse Models of Human Disease
OMIM ID Ref(s)
Alveolar Soft Part Sarcoma; ASPS 606243 J:217462




Genotype
MGI:5495301
cn5
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sortm4(EWSR1/ATF1)Mrc
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Gt(ROSA)26Sortm4(EWSR1/ATF1)Mrc mutation (0 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system

growth/size/body
• administration of tamoxifen prior to 3 weeks of age results in stunted growth

mortality/aging
• administration of tamoxifen prior to 3 weeks of age results in death by 12 weeks of age without tumor formation

neoplasm
• when tamoxifen is administered after 3 weeks of age more tumors form than without tamoxifen
• tumors most often in extremities, rib cage, and facial tissue
• tumors rare in dermis, liver, and bone
• mice develop clear cell sarcoma mimicking tumors across a broad anatomic distribution at 3-6 months of age in the absence of tamoxifen, indicating leakiness of the cre transgene
• all mice have tumors by 12 weeks regardless of treatment




Genotype
MGI:3819400
cn6
Allelic
Composition
Telo2tm1Tdl/Telo2tm1.1Tdl
Trp53tm1Tyj/Trp53tm1Tyj
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129 * 129P2/OlaHsd * 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Telo2tm1.1Tdl mutation (0 available); any Telo2 mutation (16 available)
Telo2tm1Tdl mutation (0 available); any Telo2 mutation (16 available)
Trp53tm1Tyj mutation (9 available); any Trp53 mutation (139 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• tamoxifen-treated mouse embryonic fibroblasts exhibit cell cycle arrest after 6 days in culture unlike wild-type cells




Genotype
MGI:3836424
cn7
Allelic
Composition
Aurkatm1.1Tvd/Aurkatm1.1Tvd
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sortm1Sor
Genetic
Background
involves: 129 * 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Aurkatm1.1Tvd mutation (1 available); any Aurka mutation (28 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• in MEFs at later time points after OHT treatment and serum addition cells develop large aberrant nuclei with frequent micronuclei
• in MEFS after OHT treatment and serum addition increases in the population of cells with 4N and 8N DNA content are seen
• live cell imaging indicates a median 8 h delay in mitotic entry in MEFS after OHT treatment and serum addition compared to controls
• in MEFS after OHT treatment and serum addition more cells are in prophase and most of these show an early prophase phenotype
• in MEFS after OHT treatment and serum addition almost no cells in metaphase, anaphase, and telophase are detected
• in MEFS after OHT treatment and serum addition cells in prometaphase have a monopolar spindle with closely adjacent chromosomes, the presence of these monopolar spindles activates the spindle checkpoint
• in MEFS 28 h after OHT treatment and serum addition the percent of cells positive for PH3 is increased about 3 fold compared to controls
• however, the timing of the peak in PH3 positive cells is similar to controls
• growth defect in MEFs following OHT treatment and serum addition




Genotype
MGI:3772184
cn8
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Lhx2tm1Monu/Lhx2tm1Monu
Genetic
Background
involves: 129 * 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Lhx2tm1Monu mutation (0 available); any Lhx2 mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• at E12.5, following tamoxifen treatment at E8.5, mice display an expansion of the cortical hem and a reduction in dorsal telencephalon
• at E12.5, following tamoxifen treatment at E8.5, mice display an expansion of the cortical hem and a reduction in dorsal telencephalon
• treatment with tamoxifen at E10.5 results in subtle to inapparent abnormalities in the cortical hem at E12.5




Genotype
MGI:3806251
cn9
Allelic
Composition
Droshatm1Litt/Droshatm1.1Litt
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129 * 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Droshatm1.1Litt mutation (0 available); any Drosha mutation (63 available)
Droshatm1Litt mutation (1 available); any Drosha mutation (63 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• naive CD4+ T cells release more interferon gamma than controls after cre-mediated deletion of Rnasen induced by tamoxifen treatment
• deficient CD4+ T cells are capable of differentiating into Th1 or Th2 cells




Genotype
MGI:3819399
cn10
Allelic
Composition
Telo2tm1Tdl/Telo2tm1.1Tdl
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129 * 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Telo2tm1.1Tdl mutation (0 available); any Telo2 mutation (16 available)
Telo2tm1Tdl mutation (0 available); any Telo2 mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• tamoxifen-treated mouse embryonic fibroblasts exhibit decreased DNA-damage signaling via Trp53, Cdkn1a and Chek1 compared to wild-type cells
• after 3 to 4 days in culture tamoxifen-treated mouse embryonic fibroblasts (MEFs) arrest with 2N or 4N DNA content and exhibit reduced S and M phase unlike wild-type MEFs
• after 3 to 4 days in culture tamoxifen-treated mouse embryonic fibroblasts (MEFs) exhibit a flattened senescence-like morphology unlike wild-type MEFs

homeostasis/metabolism
• tamoxifen-treated mouse embryonic fibroblasts exhibit decreased DNA-damage signaling via Trp53, Cdkn1a and Chek1 compared to wild-type cells




Genotype
MGI:3836425
cn11
Allelic
Composition
Aurkatm1.1Tvd/Aurkatm1.1Tvd
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129 * 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Aurkatm1.1Tvd mutation (1 available); any Aurka mutation (28 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• following injection of tamoxifen at E10.5 most embryonic cells appear to be in prometaphase
• following injection of tamoxifen at E10.5 embryos show a 4 fold increase in PH3 positive cells in the thymus and lungs compared to controls
• following injection of tamoxifen at E10.5 about a 3 fold increase in the percentage of apoptotic cells in the thymus and lungs is seen




Genotype
MGI:5431572
cn12
Allelic
Composition
Acvrl1tm2.1Spo/Acvrl1tm2.1Spo
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129 * 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acvrl1tm2.1Spo mutation (0 available); any Acvrl1 mutation (8 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• adult mice administered with tamoxifen die 9-21 days after a single injection
• tamoxifen treated females show a shorter survival span than males

growth/size/body
• tamoxifen treated mutants show signs of illness such as slow movements, weight loss, pale paws, and low pO2 levels from 8-10 days after tamoxifen injection

cardiovascular system
• pulmonary arteries and veins are dilated
• high vascular permeability
• uterus shows signs of arteriovenous malformations in tamoxifen treated mutants
• mutants bearing excisional wounds on the dorsal skin and ear and treated with tamoxifen form arteriovenous shunts in the blood vessels near the wounds
• arteriovenous malformations in the GI tract of tamoxifen treated mutants are located in the Peyer's patches of small intestine and appendix
• in tamoxifen treated mutants
• in tamoxifen treated mutants
• tamoxifen treated mutants show signs of hemorrhages in the lungs

digestive/alimentary system
• arteriovenous malformations in the GI tract of tamoxifen treated mutants are located in the Peyer's patches of small intestine and appendix
• tamoxifen treated mutants exhibit darkened feces indicative of the presence of blood

hematopoietic system
• in tamoxifen treated mutants
• tamoxifen treated mutants exhibit reduced hematocrit

respiratory system
• pulmonary arteries and veins are dilated
• high vascular permeability
• tamoxifen treated mutants show signs of hemorrhages in the lungs

Mouse Models of Human Disease
OMIM ID Ref(s)
Telangiectasia, Hereditary Hemorrhagic, Type 2; HHT2 600376 J:154620




Genotype
MGI:4443109
cn13
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sortm1(cre/ERT)Nat
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129 * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Trp53tm1Tyj mutation (9 available); any Trp53 mutation (139 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• hematopoietic stem and progenitor cells of irradiated mice treated with tamoxifen do not exhibit a selective advantage over cells not expressing the modified cDNA




Genotype
MGI:4443108
cn14
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sortm1(cre/ERT)Nat
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129 * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Trp53tm1Tyj mutation (9 available); any Trp53 mutation (139 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• hematopoietic stem and progenitor cells of irradiated mice treated with tamoxifen do not exhibit a selective advantage over cells not expressing the modified cDNA




Genotype
MGI:4847601
cn15
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Ptentm1Hwu/Ptentm1Hwu
Genetic
Background
involves: 129 * 129S4/SvJae * BALB/c * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Ptentm1Hwu mutation (3 available); any Pten mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most females that develop lymphomas die at about 9 weeks post-4OHT injection
• all mutants die from tumor burden by 45 weeks post-4OHT injection

neoplasm
• treatment of mice with 4OHT at 6 weeks of age to induce cre-mediated recombination results in tumor formation with a mean latency of 17 weeks
• multiple tumors are seen in 27.3% of 4OHT-treated mice
• 46.1% of females develop endometrial cancer after 4OHT treatment
• 35% of males develop intestinal cancer after 4OHT treatment, arising from the colorectum and small intestine
• 20% of males develop prostate cancer after 4OHT treatment
• prostate intraepithelial neoplasm (PIN) is observed at 4-6 weeks post 4-OHT treatment
• 76.9% incidence of lymphomas in females after 4OHT treatment
• 40% incidence of lymphomas in males after 4OHT treatment
• lymphomas mainly arise from the thymus and mesenteric lymph nodes
• all lymphomas are derived from CD3+ T-cells with either a mature appearance of small lymphocytes or large lymphoblasts
• about 50% of males and females exhibit malignant tumors at 21 weeks and 10-11 weeks after 4OHT treatment, respectively
• 10% of males and 15.4% of females develop squamous cell carcinoma of the epidermis after 4OHT treatment

digestive/alimentary system
• males develop small or large intestinal polyps at more than 35 weeks post 4OHT treatment
• 35% of males develop intestinal cancer after 4OHT treatment, arising from the colorectum and small intestine

endocrine/exocrine glands
• prostate hyperplasia is observed at 4-6 weeks post 4-OHT treatment
• 20% of males develop prostate cancer after 4OHT treatment
• prostate intraepithelial neoplasm (PIN) is observed at 4-6 weeks post 4-OHT treatment
• 76.9% incidence of lymphomas in females after 4OHT treatment
• 40% incidence of lymphomas in males after 4OHT treatment
• lymphomas mainly arise from the thymus and mesenteric lymph nodes
• all lymphomas are derived from CD3+ T-cells with either a mature appearance of small lymphocytes or large lymphoblasts

reproductive system
• prostate hyperplasia is observed at 4-6 weeks post 4-OHT treatment
• 20% of males develop prostate cancer after 4OHT treatment
• prostate intraepithelial neoplasm (PIN) is observed at 4-6 weeks post 4-OHT treatment
• most females develop endometrial hyperplasia at between 7 and 9 weeks post 4-OHT treatment

integument
• 10% of males and 15.4% of females develop squamous cell carcinoma of the epidermis after 4OHT treatment

homeostasis/metabolism
• about 50% of males and females exhibit malignant tumors at 21 weeks and 10-11 weeks after 4OHT treatment, respectively




Genotype
MGI:4421701
cn16
Allelic
Composition
Agr2tm1.1Lpkn/Agr2tm1.1Lpkn
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129 * 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Agr2tm1.1Lpkn mutation (0 available); any Agr2 mutation (7 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• in the small intestine and colon following tamoxifen treatment
• following tamoxifen treatment, enterocyte proliferation in the small intestine and colon is decreased compared to in wild-type mice
• 3 days following tamoxifen treatment, mice show loss of normal goblet cells, acute inflammatory infiltrates in the lamina propria, and further expansion of the Paneth cells unlike in wild-type mice
• 24 hours following tamoxifen treatment, the Paneth cell compartment is expanded compared to in wild-type mice
• 3 days following tamoxifen treatment, mice show loss of normal goblet cells, acute inflammatory infiltrates in the lamina propria, and further expansion of the Paneth cells compared to in wild-type mice
• tamoxifen-treated mice lack normal goblet cells unlike wild-type mice
• 3 days following tamoxifen treatment, mice show loss of normal goblet cells, acute inflammatory infiltrates in the lamina propria, and further expansion of the Paneth cells compared to in wild-type mice
• 3 days following tamoxifen treatment, mice show loss of normal goblet cells, acute inflammatory infiltrates in the lamina propria, and further expansion of the Paneth cells compared to in wild-type mice

immune system
• 3 days following tamoxifen treatment, mice show loss of normal goblet cells, acute inflammatory infiltrates in the lamina propria, and further expansion of the Paneth cells compared to in wild-type mice

endocrine/exocrine glands
• 24 hours following tamoxifen treatment, the Paneth cell compartment is expanded compared to in wild-type mice
• 3 days following tamoxifen treatment, mice show loss of normal goblet cells, acute inflammatory infiltrates in the lamina propria, and further expansion of the Paneth cells compared to in wild-type mice

cellular
• in the small intestine and colon following tamoxifen treatment
• following tamoxifen treatment, enterocyte proliferation in the small intestine and colon is decreased compared to in wild-type mice




Genotype
MGI:4420931
cn17
Allelic
Composition
Atoh1tm3Hzo/Atoh1tm1Hzo
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129 * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atoh1tm1Hzo mutation (0 available); any Atoh1 mutation (17 available)
Atoh1tm3Hzo mutation (1 available); any Atoh1 mutation (17 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• after tamoxifen treatment, the external granule cell layer is much thinner than that of control littermates
• after tamoxifen treatment, the layer is depleted of cycling immature precursors




Genotype
MGI:4420943
cn18
Allelic
Composition
Atoh1tm3Hzo/Atoh1+
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sortm1(Smo/EYFP)Amc
Genetic
Background
involves: 129 * 129S7/SvEvBrd * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atoh1tm3Hzo mutation (1 available); any Atoh1 mutation (17 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Gt(ROSA)26Sortm1(Smo/EYFP)Amc mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• ectopic masses show numerous mitotic granule neuron precursors 10 days after tamoxifen treatment
• 10 days after tamoxifen treatment, neoplastic and preneoplastic lesions in which the external granule layer lacks the normal layered structure develop in the external layer of the cerebellum
• hypertrophic 10 days after tamoxifen treatment
• 10 days after tamoxifen treatment, neoplastic and preneoplastic lesions in which the external granule layer lacks the normal layered structure develop in the external layer of the cerebellum

cellular
• ectopic masses show numerous mitotic granule neuron precursors 10 days after tamoxifen treatment




Genotype
MGI:4420935
cn19
Allelic
Composition
Atoh1tm3Hzo/Atoh1tm1Hzo
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sortm1(Smo/EYFP)Amc
Genetic
Background
involves: 129 * 129S7/SvEvBrd * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atoh1tm1Hzo mutation (0 available); any Atoh1 mutation (17 available)
Atoh1tm3Hzo mutation (1 available); any Atoh1 mutation (17 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Gt(ROSA)26Sortm1(Smo/EYFP)Amc mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• no cycling granule neuron precursor cells are detected in the external granule cell layer 10 days after tamoxifen treatment
• 10 days after tamoxifen treatment
• 10 days after tamoxifen treatment most mice have atrophic cerebella

cellular
• no cycling granule neuron precursor cells are detected in the external granule cell layer 10 days after tamoxifen treatment




Genotype
MGI:3838621
cn20
Allelic
Composition
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Pdgfratm12Sor/Pdgfra+
Genetic
Background
involves: 129 * 129/Sv * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1Rdp mutation (5 available); any Cdkn2a mutation (29 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Pdgfratm12Sor mutation (1 available); any Pdgfra mutation (45 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• all tamoxifen-treated mice develop sarcomas of the skin or muscle connective tissue after 10 to 19 weeks
• 2 tamoxifen-treated mice develop large intestinal tumors resembling undifferentiated fibrosarcomas

muscle
• tamoxifen-treated mice develop muscle fibrosis at 10 to 19 weeks of age

integument
• tamoxifen-treated mice develop skin fibrosis at 10 to 19 weeks of age

digestive/alimentary system
• after 15 weeks, tamoxifen-treated mice exhibit intestinal fibrosis




Genotype
MGI:4443111
cn21
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sortm1(cre/ERT)Nat
Tg(H2-K-BCL2)1Josd/0
Genetic
Background
involves: 129 * C3H * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Tg(H2-K-BCL2)1Josd mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• GFP+ hematopoietic stem and progenitor cells (HSPC) from irradiated mice transplanted into irradiated mice reconstitute the HSPC population exhibit a competitive advantage over HSPC from untreated mice compared with cells from similarly irradiated wild-type mice




Genotype
MGI:4415702
cn22
Allelic
Composition
Dnaic1tm1.1Leo/Dnaic1tm1.1Leo
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dnaic1tm1.1Leo mutation (0 available); any Dnaic1 mutation (25 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• following treatment with tamoxifen, cultured tracheal ciliated epithelium exhibits no ciliary activity likely due to a lack of outer dynein arms unlike similarly treated wild-type samples
• however, epithelium morphology and number of ciliated cells are normal following treatment with tamoxifen
• tamoxifen-treated mice exhibit chronic rhinosinusitis unlike wild-type mice
• however, no lung inflammation develops in tamoxifen-treated mice
• after 3 months, tamoxifen-treated mice exhibit absent mucociliary clearance in the nasopharynx and a 50% decreased in the trachea compared with wild-type mice
• after 6 months, 3 of 4 tamoxifen-treated mice exhibit no mucociliary clearance in the trachea while 1 of 4 mice exhibit a substantial reduction in clearance compared with similarly treated wild-type mice
• after 7.5 months, tamoxifen-treated mice exhibit no mucociliary clearance in the trachea compared with similarly treated wild-type mice

immune system
• tamoxifen-treated mice exhibit chronic rhinosinusitis unlike wild-type mice
• however, no lung inflammation develops in tamoxifen-treated mice

nervous system
N
• despite ciliary defects, tamoxifen-treated mice exhibit no evidence hydroencephaly

Mouse Models of Human Disease
OMIM ID Ref(s)
Ciliary Dyskinesia, Primary, 1; CILD1 244400 J:155730




Genotype
MGI:3838615
cn23
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Pdgfratm12Sor/Pdgfra+
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Pdgfratm12Sor mutation (1 available); any Pdgfra mutation (45 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 6 months after tamoxifen treatment, mice develop intestinal disease and eventually die or are sacrificed

digestive/alimentary system
• tamoxifen-treated mice exhibit partial or complete fibrosis of the small intestine and cecum unlike in wild-type mice with increased submucosal connective tissue and proportional increase in fibroblast-like cells and collagenous matrix
• tamoxifen-treated mice exhibit partial or complete fibrosis of the small intestine and cecum unlike in wild-type mice with increased submucosal connective tissue and proportional increase in fibroblast-like cells and collagenous matrix
• tamoxifen-treated mice exhibit partial or complete fibrosis of the small intestine and cecum unlike in wild-type mice with increased submucosal connective tissue and proportional increase in fibroblast-like cells and collagenous matrix
• in tamoxifen-treated mice

cardiovascular system
• in tamoxifen-treated mice

renal/urinary system
• sclerotic glomeruli in tamoxifen-treated mice
• in tamoxifen-treated mice
• enlarged glomeruli in tamoxifen-treated mice
• in tamoxifen-treated mice

neoplasm
• at between 44 and 76 weeks of age, 5 of 29 tamoxifen-treated mice develop sarcomas arising from dermis or muscle connective tissue

muscle
• in tamoxifen-treated mice

respiratory system
• around the bronchioles in tamoxifen-treated mice

integument
• in tamoxifen-treated mice




Genotype
MGI:4834588
cn24
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Tardbptm1.1Pcw/Tardbp+
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Tardbptm1.1Pcw mutation (1 available); any Tardbp mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• during the initial 3 days after cre induction by tamoxifen, all mice show decrease in body weight due to decreased food intake, but whereas controls regain recover some weight, experimental mice do not

homeostasis/metabolism
• following cre induction, animals exhibit a decreased respiratory exchange ratio (RER) indicative of pure fat oxidation compared to controls by day 6

adipose tissue
• inspection of animals dying after cre induction by tamoxifen shows loss of body fat in these mice
• analyses of carcasses show significant decreases in whole body fat mass, but not lean mass




Genotype
MGI:4834587
cn25
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Tardbptm1.1Pcw/Tardbptm1.1Pcw
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Tardbptm1.1Pcw mutation (1 available); any Tardbp mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• when cre expression is induced with a tamoxifen-containing diet (400 mg/kg of chow), mice die by day 9 post-introduction of tamoxifen

growth/size/body
• during the initial 3 days after cre induction by tamoxifen, all mice show decrease in body weight due to decreased food intake, but whereas controls regain recover some weight, experimental mice do not
• mice show a cumulative loss of body weight compared to controls following cre induction, but energy intake (cumulative food intake) is similar to controls

homeostasis/metabolism
N
• without induction of cre by tamoxifen treatment, animals are indistinguishable from controls
• increased fat oxidation after induction is basis for increased weight loss
• following cre induction, animals exhibit a decreased respiratory exchange ratio (RER) indicative of pure fat oxidation compared to controls by day 6

adipose tissue
• inspection of animals dying after cre induction by tamoxifen shows loss of body fat in these mice
• analyses of carcasses show significant decreases in whole body fat mass, but not lean mass

cellular
• increased fat oxidation after induction is basis for increased weight loss

behavior/neurological
• energy intake on day 7 is significantly higher than on day 1 after cre induction




Genotype
MGI:5775189
cn26
Allelic
Composition
Engtm2.1Hma/Engtm2.1Hma
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Engtm2.1Hma mutation (0 available); any Eng mutation (28 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mice display signs of illness in 3-4 days after the first tamoxifen injection which includes slow movement

cardiovascular system
• adults injected with tamoxifen for 3 days develop arteriovenous malformations in AAV-VEGF-induced brain angiogenic foci 8 weeks after induction, with lesions consisting of enlarged vessels (J:212952)
• tamoxifen treated adults develop arteriovenous malformations around the ear-tag wound (J:212952)
• areas of wounds in mid-dorsum and ear of tamoxifen-injected mice show the presence of arteriovenous (AV) shunts (J:227170)
• macrophages and microhemorrhage are seen around dysplastic vessels of AAV-VEGF injected, tamoxifen treated mice in the brain
• tamoxifen treated adults develop arteriovenous malformations around the ear-tag wound (J:212952)
• areas of wounds in mid-dorsum and ear of tamoxifen-injected mice show dilated and torturous vessels and the presence of arteriovenous (AV) shunts (J:227170)
• however, blood vessels away from the wound have normal morphology (J:227170)

digestive/alimentary system
• mice display signs of illness in 3-4 days after the first tamoxifen injection which includes diarrhea

homeostasis/metabolism
• tamoxifen treated adults develop arteriovenous malformations around the ear-tag wound (J:212952)
• areas of wounds in mid-dorsum and ear of tamoxifen-injected mice show dilated and torturous vessels and the presence of arteriovenous (AV) shunts (J:227170)
• however, blood vessels away from the wound have normal morphology (J:227170)
• mice display signs of illness in 3-4 days after the first tamoxifen injection which includes dehydration

mortality/aging
• mice die around day 4-10 after the first tamoxifen treatment




Genotype
MGI:5587037
cn27
Allelic
Composition
Pkd1tm2Ggg/Pkd1tm2Ggg
Gt(ROSA)26Sortm1(cre/ERT)Nat/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:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Pkd1tm2Ggg mutation (1 available); any Pkd1 mutation (68 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• pups from nursing mothers that were injected with tamoxifen to induce Pkd1 deletion in pups, show an increase in the ratio of percent kidney weight to body weight at P23




Genotype
MGI:5425617
cn28
Allelic
Composition
Gpx4tm1.1Qra/Gpx4tm1.1Qra
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gpx4tm1.1Qra mutation (1 available); any Gpx4 mutation (90 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die within 2 weeks of the 4th injection of tamoxifen (4 injections administered over an 8 day period)

growth/size/body
• starting after 3 injections of tamoxifen in mice at 6 - 9 months of age
• becomes significant 1 week after the 4th injection of tamoxifen

cellular
• 1 week after the last tamoxifen injection
• enhanced lipid peroxidation and impaired electron transport chain activity and ATP production in mitochondria 1 week after the last tamoxifen injection

behavior/neurological
• seen in tamoxifen treated mice shortly before death

nervous system
• elevated astrocyte activation in the hippocampal region 1 week after the last tamoxifen injection
• in the hippocampal region 1 week after the last tamoxifen injection

liver/biliary system
• 1 week after the last tamoxifen injection




Genotype
MGI:5302059
cn29
Allelic
Composition
Gdpd5tm1Itl/Gdpd5tm1.1Itl
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S1/Sv * 129/Sv * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gdpd5tm1.1Itl mutation (0 available); any Gdpd5 mutation (17 available)
Gdpd5tm1Itl mutation (0 available); any Gdpd5 mutation (17 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• mice treated with tamoxifen after neurogenesis (at E10.5) exhibit normal motor pool formation
• mice treated with tamoxifen at E8.5 exhibit delayed motor neuron formation compared with control mice
• at E12.5, mice treated with tamoxifen at E8.5 exhibit fewer Isl1/2+ and vasti, adductor longus and magnus, and posterior gracilis muscle motor neurons compared with control mice
• at E14.5, mice treated with tamoxifen at E8.5 exhibit fewer Isl1/2+ and vasti muscle motor neurons compared with control mice
• however, motor neurons in adductor longus and magnus and posterior gracilis muscles recover by E14.5

cellular
• mice treated with tamoxifen at E8.5 exhibit delayed motor neuron formation compared with control mice




Genotype
MGI:4948328
cn30
Allelic
Composition
Fzd4tm1Nat/Fzd4tm2.1Nat
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fzd4tm1Nat mutation (1 available); any Fzd4 mutation (7 available)
Fzd4tm2.1Nat mutation (1 available); any Fzd4 mutation (7 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• at E18.5 in mice treated with tamoxifen at E12.5 or E13.5




Genotype
MGI:3807225
cn31
Allelic
Composition
Fzd5tm1Nat/Fzd5tm2Nat
Gt(ROSA)26Sortm1(cre/ERT)Nat/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fzd5tm1Nat mutation (1 available); any Fzd5 mutation (17 available)
Fzd5tm2Nat mutation (1 available); any Fzd5 mutation (17 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• PFN in adults displays nearly complete loss of alkaline phosphatase expressing Fzd5-null neurons by 10 days after 4HT injection and cre activation, but no loss is observed in Fzd5tm2Nat/+, cre-positive control PFNs 8 days after 4HT treatment




Genotype
MGI:5587035
cn32
Allelic
Composition
Ttc21btm2c(KOMP)Wtsi/Ttc21baln
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6N
Cell Lines EPD0041_2_E09
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Ttc21baln mutation (0 available); any Ttc21b mutation (25 available)
Ttc21btm2c(KOMP)Wtsi mutation (0 available); any Ttc21b mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• an increase in cell proliferation is seen in kidney tubules of 6-week old offspring from pregnant females injected with tamoxifen at E17.5
• from P15 to P20, an increase in cell proliferation in the renal medulla is seen the offspring of females injected with tamoxifen at E17.5
• levels of cAMP are higher in cystic kidneys of the offspring of E17.5 pregnant females injected with tamoxifen
• kidney primary cilia are stunted and show accumulation of IFT88 protein in bulb-like structures at the distal tips in the offspring of E17.5 pregnant females injected with tamoxifen
• from P15 to P20, an increase in cell proliferation in the renal medulla is seen the offspring of females injected with tamoxifen at E17.5
• elevation in ratio of percent kidney weight to body weight is seen in the offspring of E17.5 pregnant females injected with tamoxifen
• dilations of loops of Henle in the kidney cortex are seen by P15 in the offspring of pregnant females injected with tamoxifen at E17.5
• dilations of proximal tubules in the kidney cortex are seen by P15 in the offspring of pregnant females injected with tamoxifen at E17.5
• when E17.5 pregnant females are injected intraperitoneally with tamoxifen to induce ubiquitous deletion of Ttc21b, the 6 week old offspring develop cystic kidney disease
• cysts seen in the offspring of E17.5 pregnant females injected with tamoxifen originate from proximal tubules, loops of Henle, and collecting ducts
• 5 week old mice injected intraperitoneally with tamoxifen do not develop kidney cysts after 3 months
• kidneys from offspring of E17.5 pregnant females grown in culture in the presence of 8-bromo-cAMP exhibit increased cystogenic potential and treatment of these cultures with Gant61, a small molecule GLI antagonist, or Sant2, a small molecule SMO antagonist, inhibitors reduces cystogenic potential

homeostasis/metabolism
• increase in BUN levels is seen in the offspring of E17.5 pregnant females injected with tamoxifen

cellular
• kidney primary cilia are stunted and show accumulation of IFT88 protein in bulb-like structures at the distal tips in the offspring of E17.5 pregnant females injected with tamoxifen
• from P15 to P20, an increase in cell proliferation in the renal medulla is seen the offspring of females injected with tamoxifen at E17.5
• an increase in cell proliferation is seen in kidney tubules of 6-week old offspring from pregnant females injected with tamoxifen at E17.5
• from P15 to P20, an increase in cell proliferation in the renal medulla is seen the offspring of females injected with tamoxifen at E17.5




Genotype
MGI:3838616
cn33
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Pdgfratm13Sor/Pdgfra+
Genetic
Background
involves: 129S4/SvJaeSor * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Pdgfratm13Sor mutation (1 available); any Pdgfra mutation (45 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 4 of 9 tamoxifen-treated mice exhibit intestinal fibrosis
• in one tamoxifen-treated mouse

renal/urinary system
• sclerotic glomeruli in tamoxifen-treated mice
• enlarged glomeruli in tamoxifen-treated mice

cardiovascular system
• in tamoxifen-treated mice

muscle
• in tamoxifen-treated mice

integument
• in some tamoxifen-treated mice




Genotype
MGI:3814551
cn34
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Ikbkbtm1Lex/Ikbkbtm1Lex
Genetic
Background
involves: 129S/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Ikbkbtm1Lex mutation (1 available); any Ikbkb mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• following tamoxifen-treatment, mouse embryonic fibroblasts (MEFs) exhibit impaired chemotaxis in response to HMGB1 compared with wild-type cells
• however, chemotaxis in response to PDGF is normal and chemotaxis is rescued by over expression of Nfkb2
• following tamoxifen-treatment, MEFs exhibit random migration in response to an HMGB1 gradient unlike wild-type cells
• 30 to 60 minutes after exposure to HMGB1, tamoxifen-treated MEFs exhibit reduced migration velocity compared with wild-type mice





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
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last database update
07/19/2016
MGI 6.04
The Jackson Laboratory