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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Vil-cre/ERT2)23Syr
transgene insertion 23, Sylvie Robine
MGI:3053826
Summary 36 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn
Tg(Vil-cre/ERT2)23Syr/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129 * C57BL/6 * CD-1 * DBA/2 MGI:5543693
cn2
Csnk1a1tm1.1Ybn/Csnk1a1+
Tg(Vil-cre/ERT2)23Syr/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129 * C57BL/6 * CD-1 * DBA/2 MGI:5543694
cn3
Cdkn1atm1Tyj/Cdkn1atm1Tyj
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn
Tg(Vil-cre/ERT2)23Syr/0
involves: 129 * C57BL/6 * CD-1 * DBA/2 MGI:5543696
cn4
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn
Tg(Vil-cre/ERT2)23Syr/0
involves: 129 * C57BL/6 * CD-1 * DBA/2 MGI:5543691
cn5
Tcf7tm1Cle/Tcf7tm1Cle
Tcf7l1tm1Efu/Tcf7l1tm1Efu
Tg(Vil-cre/ERT2)23Syr/0
involves: 129 * C57BL/6 * DBA/2 MGI:5430371
cn6
Tcf7l1tm1Efu/Tcf7l1tm1Efu
Tg(Vil-cre/ERT2)23Syr/0
involves: 129 * C57BL/6 * DBA/2 MGI:5430370
cn7
Apctm2.1Cip/Apc+
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Vil-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2 MGI:5702420
cn8
Ptentm2Mak/Ptentm2Mak
Tg(Vil-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3829450
cn9
Rbpjtm1Hon/Rbpjtm1Hon
Tg(Vil-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:3603010
cn10
Pou5f1tm1Scho/Pou5f1tm1Scho
Tg(Vil-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:3772216
cn11
Lgr4tm1.1Knis/Lgr4tm1.1Knis
Lgr5tm2.1Cle/Lgr5tm2.1Cle
Tg(Vil-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:5285825
cn12
Tcf7l2tm2.1Cle/Tcf7l2tm2.1Cle
Tg(Vil-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:5430368
cn13
Tcf7tm1Cle/Tcf7tm1Cle
Tcf7l1tm1Efu/Tcf7l1tm1Efu
Tcf7l2tm2.1Cle/Tcf7l2tm2.1Cle
Tg(Vil-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:5430369
cn14
Slc39a4tm2Gka/Slc39a4tm2Gka
Tg(Vil-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:5438021
cn15
Slc39a5tm1Gka/Slc39a5tm1Gka
Tg(Vil-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:5581458
cn16
Apctm2.1Cip/Apc+
Tg(Vil-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:5702414
cn17
Apctm2.1Cip/Apctm2.1Cip
Tg(Vil-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:5702422
cn18
Vps35tm1.1Hckn/Vps35tm1.1Hckn
Tg(Vil-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:5749127
cn19
Btrctm1Paga/Btrctm1Paga
Fbxw11tm1Ybn/Fbxw11tm1Ybn
Tg(Vil-cre/ERT2)23Syr/?
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6 * DBA/2 MGI:5568951
cn20
Btrctm1Paga/Btrc+
Fbxw11tm1Ybn/Fbxw11tm1Ybn
Tg(Vil-cre/ERT2)23Syr/?
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6 * DBA/2 MGI:5568952
cn21
Aestm1.1Mmt/Aestm1.1Mmt
Apctm1Mmt/Apc+
Tg(Vil-cre/ERT2)23Syr/0
involves: 129S2/SvPas * C57BL/6 * DBA * SJL MGI:4888016
cn22
Slc40a1tm2Nca/Slc40a1tm2Nca
Tg(Vil-cre/ERT2)23Syr/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:3771553
cn23
Tfrctm3.1Nca/Tfrctm3.1Nca
Tg(Vil-cre/ERT2)23Syr/0
involves: 129S4/SvJae * C57BL/6 * CD-1 * DBA/2 MGI:5689323
cn24
Rab11atm1.1Ngao/Rab11atm1.1Ngao
Tg(Vil-cre/ERT2)23Syr/0
involves: 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5608788
cn25
Xbp1tm2Glm/Xbp1tm2Glm
Tg(Vil-cre/ERT2)23Syr/0
involves: 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5559518
cn26
Numbtm1Zili/Numbtm1Zili
Tg(Vil-cre/ERT2)23Syr/?
involves: 129/Sv * C57BL/6 MGI:5699005
cn27
Nr5a2tm1Sjns/Nr5a2tm1Sjns
Tg(Vil-cre/ERT2)23Syr/?
involves: 129/Sv * C57BL/6 * DBA/2 * SJL MGI:3721528
cn28
Cdc25atm1Hpw/Cdc25atm1.1Hpw
Cdc25btm1Pjd/Cdc25btm1Pjd
Tg(Vil-cre/ERT2)23Syr/0
involves: 129X1/SvJ * C57BL/6 * DBA/2 MGI:4941917
cn29
Cdc25atm1Hpw/Cdc25atm1.1Hpw
Cdc25ctm1Hpw/Cdc25ctm1Hpw
Tg(Vil-cre/ERT2)23Syr/0
involves: 129X1/SvJ * C57BL/6 * DBA/2 MGI:4941916
cn30
Cdc25btm1Hpw/Cdc25btm1Pjd
Tg(Vil-cre/ERT2)23Syr/0
involves: 129X1/SvJ * C57BL/6 * DBA/2 MGI:4943329
cn31
Cdc25atm1Hpw/Cdc25atm1.1Hpw
Tg(Vil-cre/ERT2)23Syr/0
involves: 129X1/SvJ * C57BL/6 * DBA/2 MGI:4941915
cn32
Cdc25atm1Hpw/Cdc25atm1.1Hpw
Cdc25btm1Pjd/Cdc25btm1Pjd
Cdc25ctm1Hpw/Cdc25ctm1Hpw
Tg(Vil-cre/ERT2)23Syr/0
involves: 129X1/SvJ * C57BL/6 * DBA/2 MGI:4941918
cn33
Hprttm2(CAG-mCherry/Villin*)Syr/?
Vil1tm1Syr/Vil1tm1Syr
Tg(Vil-cre/ERT2)23Syr/0
involves: C57BL/6 MGI:5512865
cn34
Hprttm1(CAG-mCherry/Villin)Syr/?
Vil1tm1Syr/Vil1tm1Syr
Tg(Vil-cre/ERT2)23Syr/0
involves: C57BL/6 MGI:5512864
cn35
Rnf43tm1Cle/Rnf43tm1Cle
Znrf3tm1Cle/Znrf3tm1Cle
Tg(Vil-cre/ERT2)23Syr/0
involves: C57BL/6 * DBA/2 MGI:5439367
cx36
Xbp1tm3Glm/Xbp1tm3Glm
Tg(Vil-cre/ERT2)23Syr/0
involves: 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5441534


Genotype
MGI:5543693
cn1
Allelic
Composition
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn
Tg(Vil-cre/ERT2)23Syr/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129 * C57BL/6 * CD-1 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Csnk1a1tm1.1Ybn mutation (1 available); any Csnk1a1 mutation (28 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (147 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• after 2 weeks of tamoxifen treatment

tumorigenesis
• widespread high-grade dysplasia and numerous intramucosal carcinomas invading the lamina propria in most of the small-bowel crypts and villi within 2 weeks of tamoxifen treatment

digestive/alimentary system
• increased proliferation after tamoxifen treatment throughout the crypt-villus axis

cellular
• in the gut of tamoxifen treated mice but no more so than in Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn Tg(Vil-cre/ERT2)23Syr mice
• increased proliferation after tamoxifen treatment throughout the crypt-villus axis




Genotype
MGI:5543694
cn2
Allelic
Composition
Csnk1a1tm1.1Ybn/Csnk1a1+
Tg(Vil-cre/ERT2)23Syr/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129 * C57BL/6 * CD-1 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Csnk1a1tm1.1Ybn mutation (1 available); any Csnk1a1 mutation (28 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (147 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• within 6 months, 7 of 9 tamoxifen-treated mice develop invasive carcinomas that permeates the bowel muscular wall into the subserosal fat with some involvement of the serosal surface (stage T4)




Genotype
MGI:5543696
cn3
Allelic
Composition
Cdkn1atm1Tyj/Cdkn1atm1Tyj
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129 * C57BL/6 * CD-1 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn1atm1Tyj mutation (3 available); any Cdkn1a mutation (46 available)
Csnk1a1tm1.1Ybn mutation (1 available); any Csnk1a1 mutation (28 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• tamoxifen-treated mice exhibit severe dysplasia and intramucosal carcinomas throughout the small bowel

digestive/alimentary system
• massive proliferation in the villi compartment in tamoxifen-treated mice

cellular
• massive proliferation in the villi compartment in tamoxifen-treated mice




Genotype
MGI:5543691
cn4
Allelic
Composition
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129 * C57BL/6 * CD-1 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Csnk1a1tm1.1Ybn mutation (1 available); any Csnk1a1 mutation (28 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• in the gut following tamoxifen treatment
• in mouse embryonic fibroblasts following tamoxifen treatment




Genotype
MGI:5430371
cn5
Allelic
Composition
Tcf7tm1Cle/Tcf7tm1Cle
Tcf7l1tm1Efu/Tcf7l1tm1Efu
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tcf7l1tm1Efu mutation (0 available); any Tcf7l1 mutation (71 available)
Tcf7tm1Cle mutation (0 available); any Tcf7 mutation (8 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• tamoxifen-treated mice exhibit normal adult intestinal homeostasis




Genotype
MGI:5430370
cn6
Allelic
Composition
Tcf7l1tm1Efu/Tcf7l1tm1Efu
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tcf7l1tm1Efu mutation (0 available); any Tcf7l1 mutation (71 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• tamoxifen-treated mice exhibit normal adult intestinal homeostasis




Genotype
MGI:5702420
cn7
Allelic
Composition
Apctm2.1Cip/Apc+
Atg7tm1Tchi/Atg7tm1Tchi
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2.1Cip mutation (2 available); any Apc mutation (85 available)
Atg7tm1Tchi mutation (1 available); any Atg7 mutation (19 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• tamoxifen treated mice show fewer and smaller colonic tumors that develop more slowly and have a lower proliferation rate than in single conditional Apc heterozygous mice
• however, prolonged antibiotic treatment of tamoxifen treated mice induces numerous intestinal tumor foci and tamoxifen treated mice administered anti-CD8 antibodies to induce partial depletion of Treg show increased tumor development

digestive/alimentary system
• unusually small in tumor-free mucosa of tamoxifen treated mice
• abnormal accumulation of granules of mucus in goblet cells in the tumor-free mucosa of tamoxifen treated mice
• tamoxifen treated mice show fewer and smaller colonic tumors that develop more slowly and have a lower proliferation rate than in single conditional Apc heterozygous mice
• however, prolonged antibiotic treatment of tamoxifen treated mice induces numerous intestinal tumor foci and tamoxifen treated mice administered anti-CD8 antibodies to induce partial depletion of Treg show increased tumor development
• tamoxifen treated mice show altered distribution of gut bacteria, with bacteria occasionally seen within the crypt compartment of the small intestine
• tamoxifen treated mice show a difference in the overall composition of both fecal and ileal microbiota compared to single conditional Apc heterozygotes, with mice showing a high level of Gram+ bacteria related to Firmicutes and low levels of Proteobacteria in feces
• ileal mucosa of tamoxifen treated mice has a higher bacterial diversity than single conditional Apc heterozygotes
• intestinal permeability is high in tamoxifen treated mice

endocrine/exocrine glands
• unusually small in tumor-free mucosa of tamoxifen treated mice

hematopoietic system
• proportion of CD103+CD11b- dendritic cell subset involved in T-cell priming is higher in tamoxifen treated mice than in single conditional Apc heterozygous mice
• the number of Treg and CD8 IFN-gamma T cells in the lamina propria is higher than in single conditional Apc heterozygous mice
• administration of IL-1beta receptor antagonist, anakinra, to tamoxifen treated mice is sufficient to prevent the expansion of cytotoxic CD8+ T cells
• the number of Treg and CD8 IFN-gamma T cells in the lamina propria is higher than in single conditional Apc heterozygous mice

immune system
• proportion of CD103+CD11b- dendritic cell subset involved in T-cell priming is higher in tamoxifen treated mice than in single conditional Apc heterozygous mice
• the number of Treg and CD8 IFN-gamma T cells in the lamina propria is higher than in single conditional Apc heterozygous mice
• administration of IL-1beta receptor antagonist, anakinra, to tamoxifen treated mice is sufficient to prevent the expansion of cytotoxic CD8+ T cells
• the number of Treg and CD8 IFN-gamma T cells in the lamina propria is higher than in single conditional Apc heterozygous mice
• tamoxifen treated mice show marked infiltration of lymphocytes within the normal mucosa, higher numbers of CD45 and T cells in the small intestine and colon mucosa, influx of CD11c+ cells in the intestinal mucosa compared to single conditional Apc heterozygous mice, indicating promotion of anti-tumor immune responses
• immune cells isolated from the lamina propria of tamoxifen treated mice produce high amounts of IL-1beta
• immune cells isolated from the lamina propria of tamoxifen treated mice produce high amounts of IL-10




Genotype
MGI:3829450
cn8
Allelic
Composition
Ptentm2Mak/Ptentm2Mak
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2Mak mutation (2 available); any Pten mutation (40 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• following induction with tamoxifen in utero or in adult mice, crypt-villi architecture and physiology are normal

integument
• when induced with tamoxifen in utero, mice develop a shaggy or ruffled coat




Genotype
MGI:3603010
cn9
Allelic
Composition
Rbpjtm1Hon/Rbpjtm1Hon
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rbpjtm1Hon mutation (2 available); any Rbpj mutation (187 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 6 days after the last injection of tamoxifen (given for 5 consecutive days), in the small intestine and colon the rapidly dividing transit amplifying compartment is replaced by post-mitotic goblet cells, with almost complete conversion by 12 days

endocrine/exocrine glands
• 6 days after the last injection of tamoxifen (given for 5 consecutive days), in the small intestine and colon the rapidly dividing transit amplifying compartment is replaced by post-mitotic goblet cells, with almost complete conversion by 12 days




Genotype
MGI:3772216
cn10
Allelic
Composition
Pou5f1tm1Scho/Pou5f1tm1Scho
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pou5f1tm1Scho mutation (0 available); any Pou5f1 mutation (72 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• mutants display normal intestinal tissue architecture, crypt regenerative capacity after irradiation, and normal weight gain




Genotype
MGI:5285825
cn11
Allelic
Composition
Lgr4tm1.1Knis/Lgr4tm1.1Knis
Lgr5tm2.1Cle/Lgr5tm2.1Cle
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr4tm1.1Knis mutation (0 available); any Lgr4 mutation (67 available)
Lgr5tm2.1Cle mutation (0 available); any Lgr5 mutation (12 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• generated intestinal organoids degrade after 2 days of tamoxifen treatment
• however, organoid survival is rescued by retroviral expression of LGR5




Genotype
MGI:5430368
cn12
Allelic
Composition
Tcf7l2tm2.1Cle/Tcf7l2tm2.1Cle
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tcf7l2tm2.1Cle mutation (0 available); any Tcf7l2 mutation (21 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• between day 1 and 5 of tamoxifen treatment
• tamoxifen-treated mice exhibit an absence of proliferative cells in the adult small intestine after 7 days of treatment
• cultured intestinal organoids treated with tamoxifen exhibit a block in proliferation and subsequent death of the organoid by day 6
• 3 days after tamoxifen treatment, mice exhibit an elimination in Olfm4+ intestinal stem cells with the exception of in escaper crypts
• 3 days after tamoxifen treatment, the small remaining Ki67+ escaper crypts contain limited numbers of correctly localized lysozyme-positive Paneth cells
• 7 days after tamoxifen treatment, essentially all lysozyme-positive Paneth cells are eliminated
• 3 days after tamoxifen treatment, Paneth cells are eliminated from the crypt of Lieberkuhn and aberrantly located on the villi
• 3 days after tamoxifen treatment, some goblet cells express Paneth cell markers

cellular
• between day 1 and 5 of tamoxifen treatment
• tamoxifen-treated mice exhibit an absence of proliferative cells in the adult small intestine after 7 days of treatment
• cultured intestinal organoids treated with tamoxifen exhibit a block in proliferation and subsequent death of the organoid by day 6

endocrine/exocrine glands
• 3 days after tamoxifen treatment, the small remaining Ki67+ escaper crypts contain limited numbers of correctly localized lysozyme-positive Paneth cells
• 7 days after tamoxifen treatment, essentially all lysozyme-positive Paneth cells are eliminated
• 3 days after tamoxifen treatment, Paneth cells are eliminated from the crypt of Lieberkuhn and aberrantly located on the villi




Genotype
MGI:5430369
cn13
Allelic
Composition
Tcf7tm1Cle/Tcf7tm1Cle
Tcf7l1tm1Efu/Tcf7l1tm1Efu
Tcf7l2tm2.1Cle/Tcf7l2tm2.1Cle
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tcf7l1tm1Efu mutation (0 available); any Tcf7l1 mutation (71 available)
Tcf7l2tm2.1Cle mutation (0 available); any Tcf7l2 mutation (21 available)
Tcf7tm1Cle mutation (0 available); any Tcf7 mutation (8 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• tamoxifen-treatment results in the same defects as in Tcf7l2tm2.1Cle/Tcf7l2tm2.1Cle Tg(Vil-cre/ERT2)23Syr mice
• tamoxifen-treatment results in the same defects as in Tcf7l2tm2.1Cle/Tcf7l2tm2.1Cle Tg(Vil-cre/ERT2)23Syr mice




Genotype
MGI:5438021
cn14
Allelic
Composition
Slc39a4tm2Gka/Slc39a4tm2Gka
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc39a4tm2Gka mutation (1 available); any Slc39a4 mutation (11 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Growth retardation of tamoxifen treated Slc39a4tm2Gka/Slc39a4tm2Gka Tg(Vil-cre/ERT2)23Syr/0 mice

mortality/aging
• mice treated with tamoxifen as neonates die within a week of weaning unless excess zinc is provided in the drinking water
• mice treated with tamoxifen (3 injections) 5 days after weaning die unless provided with excess zinc in the drinking water
• removal of excess zinc in the drinking water results in precipitous weight loss and death in mice treated with tamoxifen as neonates or after weaning
• excess zinc must be provided by day 6 after tamoxifen treatment to prevent lethality
• mice treated with tamoxifen at 7 weeks of age die around 1 week after the treatment

growth/size/body
• rapid weight loss after weaning in mice treated with tamoxifen as neonates unless excess zinc is provided in the drinking water
• rapid weight loss is seen within a few days of tamoxifen treatment in mice treated with tamoxifen (3 injections) 5 days after weaning despite normal food consumption and much of this weight loss involves loss of muscle and bone
• mice given a single injection of tamoxifen after weaning slowly lose weight, about half recover and resume normal growth
• rapid weight loss is also seen when mice are treated with tamoxifen at 7 weeks of age
• mice treated with tamoxifen as neonates provided excess zinc in the drinking water at weaning still fail to gain much body weight following weaning

homeostasis/metabolism
• increase in manganese in the liver by 4 days after tamoxifen treatment with levels about twice normal by 8 days after treatment
• about a 50% decrease in copper levels in the small intestine by 4 days after tamoxifen treatment
• decrease in copper levels in the pancreas by 4 days after tamoxifen treatment
• by 4 days after tamoxifen treatment
• largest loss of copper occurs in the small intestine
• by 4 days after tamoxifen treatment
• by 8 days after tamoxifen treatment
• levels are about twice normal by 8 days after tamoxifen treatment
• decrease in zinc levels in the small intestine, pancreas and liver at 4 days after tamoxifen treatment
• decrease in zinc levels correlates with the beginning of weight loss
• levels in the liver normalize by 8 days after tamoxifen treatment

digestive/alimentary system
• decrease in proliferation at 2, 4 and 6 days after tamoxifen treatment
• progressive and profound disorganization of the crypt architecture after tamoxifen treatment
• crypts become elongated 2 days after tamoxifen treatment
• after tamoxifen treatment Paneth cells contain large cytoplasmic vacuoles and the store of labile zinc is rapidly depleted
• about a 50% decrease in copper levels in the small intestine by 4 days after tamoxifen treatment
• progressive and profound disorganization of the villus after tamoxifen treatment
• by 6 days after tamoxifen treatment epithelial cells have lost much of their columnar morphology becoming cuboidal with centric nuclei
• by 6 days after tamoxifen treatment the lamina propria appears disorganized, occupies more space in the villi, and often contains red blood cells and cells with pyknotic nuclei

liver/biliary system
• increase in manganese in the liver by 4 days after tamoxifen treatment with levels about twice normal by 8 days after treatment
• by 4 days after tamoxifen treatment
• by 8 days after tamoxifen treatment
• levels are about twice normal by 8 days after tamoxifen treatment

muscle
• rapid muscle weight loss is seen within a few days of tamoxifen treatment in mice treated with tamoxifen 5 days after weaning despite normal food consumption

skeleton
• loss of bone mass is seen within a few days of tamoxifen treatment in mice treated with tamoxifen 5 days after weaning despite normal food consumption

cellular
• decrease in proliferation at 2, 4 and 6 days after tamoxifen treatment

endocrine/exocrine glands
• progressive and profound disorganization of the crypt architecture after tamoxifen treatment
• crypts become elongated 2 days after tamoxifen treatment
• after tamoxifen treatment Paneth cells contain large cytoplasmic vacuoles and the store of labile zinc is rapidly depleted

Mouse Models of Human Disease
OMIM ID Ref(s)
Acrodermatitis Enteropathica, Zinc-Deficiency Type; AEZ 201100 J:187178




Genotype
MGI:5581458
cn15
Allelic
Composition
Slc39a5tm1Gka/Slc39a5tm1Gka
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc39a5tm1Gka mutation (1 available); any Slc39a5 mutation (11 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• tamoxifen-treated mice provided adequate or excess zinc (by diet or gavage) exhibit increased pancreatic zinc compared with control mice




Genotype
MGI:5702414
cn16
Allelic
Composition
Apctm2.1Cip/Apc+
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2.1Cip mutation (2 available); any Apc mutation (85 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• tamoxifen treated mice develop intestinal adenomas after the sporadic loss of the remaining Apc allele
• tamoxifen treated mice develop colon adenomas after the sporadic loss of the remaining Apc allele

mortality/aging
• tamoxifen treated mice show signs of illness and have to be euthanized at 135 days due to large tumor burden

growth/size/body
• tamoxifen treated mice show loss of body weight, pale feet and hunching

digestive/alimentary system
• tumors of tamoxifen treated mice in the distal colon and rectum are associated with frequent rectal prolapse
• in tamoxifen treated mice
• prolonged antibiotic administration of tamoxifen treated mice does not affect severity of polyposis
• metaformin treatment impairs the growth of polyps in tamoxifen-treated mice but does not affect adenoma cell proliferation
• tamoxifen treated mice develop intestinal adenomas after the sporadic loss of the remaining Apc allele
• tamoxifen treated mice show a difference in the overall composition of both fecal and ileal microbiota compared to double conditional mice heterozygous for Apc and homozygous for Atg7, with mice showing high levels of Gram- bacteria mostly from Helicobacter in the feces
• ileal mucosa of tamoxifen treated mice has a lower bacterial diversity than in double conditional mice heterozygous for Apc and homozygous for Atg7
• the ratio of Gram- to Gram+ bacteria is lower in tamoxifen treated mice than in double conditional mice heterozygous for Apc and homozygous for Atg7

cellular
• tamoxifen-treated mice show activation of autophagy in tumoral cells

Mouse Models of Human Disease
OMIM ID Ref(s)
Colorectal Cancer; CRC 114500 J:227287




Genotype
MGI:5702422
cn17
Allelic
Composition
Apctm2.1Cip/Apctm2.1Cip
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2.1Cip mutation (2 available); any Apc mutation (85 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice appear unwell and are moribund 4 days after tamoxifen injection

digestive/alimentary system
• tamoxifen treated mice show numerous apoptotic bodies in the crypts and higher number of apoptotic cells in the elongated crypts
• marker analysis indicates that the intestinal mucosa of tamoxifen treated mice lacks differentiation into enterocytes, goblet, or enteroendocrine cells and is committed to the Paneth cell lineage, although most of the cells do not show typical granules indicating that they do not undergo full differentiation to the Paneth cell lineage
• tamoxifen treated mice exhibit an increase in cell proliferation in intestinal epithelium
• tamoxifen treated mice show slowed migration of epithelial cells along the crypt-villus axis in the epithelium
• tamoxifen treated mice show dysplasia in the crypt all along the small intestine, including pseudostratification, enlargement of the nuclei, prominent nucleoli, and basophil accumulation
• the crypt compartment of tamoxifen treated mice is greatly expanded
• goblet cells are less numerous in the intestinal epithelium of tamoxifen treated mice
• tamoxifen treated mice show some rare lesions in the proximal colon which show characteristics similar to the small intestinal dysplasia

endocrine/exocrine glands
• tamoxifen treated mice show dysplasia in the crypt all along the small intestine, including pseudostratification, enlargement of the nuclei, prominent nucleoli, and basophil accumulation
• the crypt compartment of tamoxifen treated mice is greatly expanded

cellular
• tamoxifen treated mice show numerous apoptotic bodies in the crypts and higher number of apoptotic cells in the elongated crypts




Genotype
MGI:5749127
cn18
Allelic
Composition
Vps35tm1.1Hckn/Vps35tm1.1Hckn
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
Vps35tm1.1Hckn mutation (0 available); any Vps35 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

4-hydroxytamoxifen treated Vps35tm1.1Hckn/Vps35tm1.1Hckn Tg(Vil-cre/ERT2)23Syr/0 mice exhibit no differences in small intestine crypt or villus morphology

digestive/alimentary system
N
• at 3 days, 1 week, 4 weeks and 8 weeks after 4-hydroxytamoxifen (4-OHT) injection, adult mice exhibit no differences in crypt or villus morphology in the small intestine relative to control littermates
• in culture, 4-OHT-treated small intestinal crypt organoids show reduced Wntless (Wls) protein levels but exhibit normal overall morphology, with Paneth cells visible at the tips of the bud, and can grow for many passages without Wnt supplementation in the growth medium
• 4-OHT-treated intestinal organoids show normal survival rates in different R-spondin concentrations
• 5 days after passaging, 4-OHT-treated intestinal organoids develop fewer crypt-like buds relative to control organoids, indicating a mild proliferation defect
• supplementation of exogenous Wnt3a in the medium does not fully rescue this growth defect, although 4-OHT-treated organoids can respond to Wnt signaling

cellular
• 5 days after passaging, 4-OHT-treated intestinal organoids develop fewer crypt-like buds relative to control organoids, indicating a mild proliferation defect
• supplementation of exogenous Wnt3a in the medium does not fully rescue this growth defect, although 4-OHT-treated organoids can respond to Wnt signaling




Genotype
MGI:5568951
cn19
Allelic
Composition
Btrctm1Paga/Btrctm1Paga
Fbxw11tm1Ybn/Fbxw11tm1Ybn
Tg(Vil-cre/ERT2)23Syr/?
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Btrctm1Paga mutation (2 available); any Btrc mutation (36 available)
Fbxw11tm1Ybn mutation (0 available); any Fbxw11 mutation (49 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• appearance of severe diarrhea and rectal bleeding in mice given tamoxifen is followed by death within 24 hours
• wide gaps in epithelial tight junctions found in enterocytes following tamoxifen administration
• loss of most epithelial cells in large intestine following tamoxifen administration
• remaining mucosa is infiltrated with inflammatory and immune cells
• intestinal barrier disruption observed as early as 24 hours after tamoxifen treatment
• unrecognizable crypt structures in large intestine by day 5 following tamoxifen administration
• mice develop severe colitis following tamoxifen administration
• loss of most epithelial cells in large intestine following tamoxifen administration
• remaining mucosa is infiltrated with inflammatory and immune cells
• appearance of severe diarrhea and rectal bleeding in mice given tamoxifen is followed by death within 24 hours
• inflammation in small and large intestines following tamoxifen administration

cellular
• mitosis is abnormally prolonged in enterocytes following tamoxifen administration
• more than 2 centrosomes observed in enterocytes following tamoxifen administration
• mitotic enterocytes have abnormal spindles following tamoxifen administration
• observed in enterocytes following tamoxifen administration

cardiovascular system
• appearance of severe diarrhea and rectal bleeding in mice given tamoxifen is followed by death within 24 hours

endocrine/exocrine glands
• unrecognizable crypt structures in large intestine by day 5 following tamoxifen administration

homeostasis/metabolism
• increase in IL1b levels beginning day 1 and spiking on day 3 following tamoxifen administration

immune system
• inflammation in small and large intestines following tamoxifen administration
• increase in IL1b levels beginning day 1 and spiking on day 3 following tamoxifen administration

mortality/aging
• appearance of severe diarrhea and rectal bleeding in mice given tamoxifen is followed by death within 24 hours




Genotype
MGI:5568952
cn20
Allelic
Composition
Btrctm1Paga/Btrc+
Fbxw11tm1Ybn/Fbxw11tm1Ybn
Tg(Vil-cre/ERT2)23Syr/?
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Btrctm1Paga mutation (2 available); any Btrc mutation (36 available)
Fbxw11tm1Ybn mutation (0 available); any Fbxw11 mutation (49 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• severe inflammation and a disrupted epithelial layer occurs 4 days after tamoxifen administration
• wide gaps in enterocyte epithelial tight junctions following tamoxifen administration
• mucositis observed in colon following tamoxifen administration
• spontaneous recovery occurs 3 weeks after tamoxifen administration




Genotype
MGI:4888016
cn21
Allelic
Composition
Aestm1.1Mmt/Aestm1.1Mmt
Apctm1Mmt/Apc+
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * DBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Aestm1.1Mmt mutation (0 available); any Aes mutation (8 available)
Apctm1Mmt mutation (0 available); any Apc mutation (85 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• adenocarcinomas by histopathological definition
• the extent of cellular atypia and epithelial architecture are rather similar to those in the Apctm1Mmt adenomas, without a very malignant appearance
• adenocarcinomas by histopathological definition
• the extent of cellular atypia and epithelial architecture are rather similar to those in the Apctm1Mmt adenomas, without a very malignant appearance

tumorigenesis
• adenocarcinomas by histopathological definition
• the extent of cellular atypia and epithelial architecture are rather similar to those in the Apctm1Mmt adenomas, without a very malignant appearance
• adenocarcinomas by histopathological definition
• the extent of cellular atypia and epithelial architecture are rather similar to those in the Apctm1Mmt adenomas, without a very malignant appearance
• treated with 4-hydroxytamoxifen to activate Cre recombinase at 3 weeks of age
• tumor invasion and intravasation into the smooth muscle layer of the small intestine and colon at 17 weeks of age
• in polyps larger than 2 mm in diameter, about half of them is found invading into the submucosa or beyond
• often seen inside vessels that are distended, reminiscent of tumor embolism




Genotype
MGI:3771553
cn22
Allelic
Composition
Slc40a1tm2Nca/Slc40a1tm2Nca
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc40a1tm2Nca mutation (1 available); any Slc40a1 mutation (17 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• visibly anemic by 8 days after the first tamoxifen injection
• severe iron deficient anemia develops by 6 - 7 weeks after the start of tamoxifen treatment
• by 6 - 7 weeks after the start of tamoxifen treatment, average hematocrit is 11.2 +/- 1.6% compared to 45.3 +/- 5.9% in controls without the cre transgene
• parenteral treatment with iron dextran restores hematocrits in tamoxifen treated mice to levels similar to control mice that do not carry the cre transgene
• by 6 - 7 weeks after the start of tamoxifen treatment, average hemoglobin concentration is 2.8 +/- 0.6 g/dl compared to 13.8 +/- 1.8 g/dl in controls without the cre transgene
• a 4.7-fold decrease in splenic nonheme iron is seen after tamoxifen treatment

homeostasis/metabolism
• significant iron accumulation in duodenal enterocytes after tamoxifen treatment
• a 4.7-fold decrease in splenic nonheme iron is seen after tamoxifen treatment
• a 5.5-fold decrease in hepatic nonheme iron is seen after tamoxifen treatment

digestive/alimentary system
• significant iron accumulation in duodenal enterocytes after tamoxifen treatment

immune system
• a 4.7-fold decrease in splenic nonheme iron is seen after tamoxifen treatment

liver/biliary system
• a 5.5-fold decrease in hepatic nonheme iron is seen after tamoxifen treatment




Genotype
MGI:5689323
cn23
Allelic
Composition
Tfrctm3.1Nca/Tfrctm3.1Nca
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CD-1 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tfrctm3.1Nca mutation (2 available); any Tfrc mutation (25 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice are killed 1-3 days after the last tamoxifen dose due to poor health
• treatment with iron dextran does not extend lifespan in tamoxifen-treated mice

digestive/alimentary system
• reduced proliferation in tamoxifen-treated mice
• blunted villi in tamoxifen-treated mice
• in tamoxifen-treated mice
• on the fourth day of tamoxifen treatment

growth/size/body
• on the fourth day of tamoxifen treatment

cellular
• reduced proliferation in tamoxifen-treated mice




Genotype
MGI:5608788
cn24
Allelic
Composition
Rab11atm1.1Ngao/Rab11atm1.1Ngao
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rab11atm1.1Ngao mutation (1 available); any Rab11a mutation (7 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• adult mice administered tamoxifen exhibit increased crypt cell proliferation

digestive/alimentary system
• adult mice administered tamoxifen exhibit increased crypt cell proliferation

immune system
• intestinal organoid cultures induced with tamoxifen produce a 2-fold increase in interleukin-6 secretion




Genotype
MGI:5559518
cn25
Allelic
Composition
Xbp1tm2Glm/Xbp1tm2Glm
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
Xbp1tm2Glm mutation (0 available); any Xbp1 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• treatment of mice with rapamycin reduces severity of enteritis

digestive/alimentary system
• intenstinal epithelial cells exhibit ER (endoplamic reticulum) stress by 3 days after tamoxifen treatment
• treatment of mice with rapamycin reduces severity of enteritis

cellular
• autophagy is induced in enterocytes, most notably in Paneth cells by 3 days after tamoxifen treatment
• treatment of mice with rapamycin induces autophagy in Paneth cells




Genotype
MGI:5699005
cn26
Allelic
Composition
Numbtm1Zili/Numbtm1Zili
Tg(Vil-cre/ERT2)23Syr/?
Genetic
Background
involves: 129/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Numbtm1Zili mutation (3 available); any Numb mutation (43 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• cholesterol endocytosis fails in tamoxifen treated mice
• less cholesterol absorption in liver
• lower plasma cholesterol levels in tamoxifen treated mice
• partial resistance to diet induced hypercholesterolemia

digestive/alimentary system
• cholesterol endocytosis fails in tamoxifen treated mice
• less cholesterol absorption in liver




Genotype
MGI:3721528
cn27
Allelic
Composition
Nr5a2tm1Sjns/Nr5a2tm1Sjns
Tg(Vil-cre/ERT2)23Syr/?
Genetic
Background
involves: 129/Sv * C57BL/6 * DBA/2 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nr5a2tm1Sjns mutation (0 available); any Nr5a2 mutation (80 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• following treatment with tamoxifen, 2,4,6-trinitrobezene sulfonic acid (TNBS)-induced colitis results in severe lesions with advanced necrosis
• following treatment with tamoxifen, 2,4,6-trinitrobezene sulfonic acid (TNBS)-induced colitis is more severe than in wild-type mice

immune system
• following treatment with tamoxifen, 2,4,6-trinitrobezene sulfonic acid (TNBS)-induced colitis is more severe than in wild-type mice




Genotype
MGI:4941917
cn28
Allelic
Composition
Cdc25atm1Hpw/Cdc25atm1.1Hpw
Cdc25btm1Pjd/Cdc25btm1Pjd
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdc25atm1.1Hpw mutation (1 available); any Cdc25a mutation (15 available)
Cdc25atm1Hpw mutation (1 available); any Cdc25a mutation (15 available)
Cdc25btm1Pjd mutation (0 available); any Cdc25b mutation (10 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 2 of 5 tamoxifen-treated mice die by day 8

digestive/alimentary system
• in tamoxifen-treated mice
• tamoxifen-treated mice exhibit premature differentiation of small intestine crypt cells compared with control mice
• tamoxifen-treated mice exhibit decreased S-phase cells in crypts compared with control mice
• reduced length in tamoxifen-treated mice
• reduced length in tamoxifen-treated mice
• tamoxifen treated mice exhibit a reduction in epithelium cells in the small intestine crypts compared with control mice
• however, the number of Paneth cells is normal
• in tamoxifen-treated mice

growth/size/body
• in tamoxifen-treated mice

endocrine/exocrine glands
• tamoxifen treated mice exhibit a reduction in epithelium cells in the small intestine crypts compared with control mice
• however, the number of Paneth cells is normal

cellular
• in tamoxifen-treated mice
• tamoxifen-treated mice exhibit premature differentiation of small intestine crypt cells compared with control mice
• tamoxifen-treated mice exhibit decreased S-phase cells in crypts compared with control mice




Genotype
MGI:4941916
cn29
Allelic
Composition
Cdc25atm1Hpw/Cdc25atm1.1Hpw
Cdc25ctm1Hpw/Cdc25ctm1Hpw
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdc25atm1.1Hpw mutation (1 available); any Cdc25a mutation (15 available)
Cdc25atm1Hpw mutation (1 available); any Cdc25a mutation (15 available)
Cdc25ctm1Hpw mutation (1 available); any Cdc25c mutation (16 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• tamoxifen-treated mice exhibit normal intestine morphology

growth/size/body
N
• tamoxifen-treated mice exhibit normal body weight




Genotype
MGI:4943329
cn30
Allelic
Composition
Cdc25btm1Hpw/Cdc25btm1Pjd
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdc25btm1Hpw mutation (1 available); any Cdc25b mutation (10 available)
Cdc25btm1Pjd mutation (0 available); any Cdc25b mutation (10 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• tamoxifen-treated mice exhibit normal intestine morphology

growth/size/body
N
• tamoxifen-treated mice exhibit normal body weight




Genotype
MGI:4941915
cn31
Allelic
Composition
Cdc25atm1Hpw/Cdc25atm1.1Hpw
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdc25atm1.1Hpw mutation (1 available); any Cdc25a mutation (15 available)
Cdc25atm1Hpw mutation (1 available); any Cdc25a mutation (15 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mild reduction in length in tamoxifen-treated mice
• mild reduction in length in tamoxifen-treated mice

growth/size/body
N
• tamoxifen-treated mice exhibit normal body weight




Genotype
MGI:4941918
cn32
Allelic
Composition
Cdc25atm1Hpw/Cdc25atm1.1Hpw
Cdc25btm1Pjd/Cdc25btm1Pjd
Cdc25ctm1Hpw/Cdc25ctm1Hpw
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdc25atm1.1Hpw mutation (1 available); any Cdc25a mutation (15 available)
Cdc25atm1Hpw mutation (1 available); any Cdc25a mutation (15 available)
Cdc25btm1Pjd mutation (0 available); any Cdc25b mutation (10 available)
Cdc25ctm1Hpw mutation (1 available); any Cdc25c mutation (16 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 5 of 11 tamoxifen-treated mice die by day 8

digestive/alimentary system
• in tamoxifen-treated mice
• tamoxifen-treated mice exhibit premature differentiation of small intestine crypt cells compared with control mice
• tamoxifen-treated mice exhibit decreased S-phase cells in crypts compared with control mice
• reduced length in tamoxifen-treated mice
• reduced length in tamoxifen-treated mice
• tamoxifen treated mice exhibit a reduction in epithelium cells in the small intestine crypts compared with control mice
• however, the number of Paneth cells is normal
• in tamoxifen-treated mice

growth/size/body
• in tamoxifen-treated mice

endocrine/exocrine glands
• tamoxifen treated mice exhibit a reduction in epithelium cells in the small intestine crypts compared with control mice
• however, the number of Paneth cells is normal

cellular
• in tamoxifen-treated mice
• tamoxifen-treated mice exhibit premature differentiation of small intestine crypt cells compared with control mice
• tamoxifen-treated mice exhibit decreased S-phase cells in crypts compared with control mice




Genotype
MGI:5512865
cn33
Allelic
Composition
Hprttm2(CAG-mCherry/Villin*)Syr/?
Vil1tm1Syr/Vil1tm1Syr
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hprttm2(CAG-mCherry/Villin*)Syr mutation (0 available); any Hprt mutation (1256 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
Vil1tm1Syr mutation (0 available); any Vil1 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• failure to heal properly at 3 and 7 days after carbachol treatment in tamoxifen induced mice
• very few cells in contact with sodium deoxycholate induced injury show polarity loss




Genotype
MGI:5512864
cn34
Allelic
Composition
Hprttm1(CAG-mCherry/Villin)Syr/?
Vil1tm1Syr/Vil1tm1Syr
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hprttm1(CAG-mCherry/Villin)Syr mutation (0 available); any Hprt mutation (1256 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
Vil1tm1Syr mutation (0 available); any Vil1 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• after tamoxifen induction
• injury repair after carbachol treatment is complete after 7 days as in control mice
• columnar epithelium begins to flatten 30 minutes after injury with sodium deoxycholate
• apico-basal polarity lost, microvillus disassembly




Genotype
MGI:5439367
cn35
Allelic
Composition
Rnf43tm1Cle/Rnf43tm1Cle
Znrf3tm1Cle/Znrf3tm1Cle
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rnf43tm1Cle mutation (0 available); any Rnf43 mutation (17 available)
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
Znrf3tm1Cle mutation (0 available); any Znrf3 mutation (19 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• following tamoxifen treatment a marked expansion of the proliferative compartment is seen
• following tamoxifen treatment a marked expansion of the proliferative compartment is seen with enlarged crypts and Ki67+ cells ectopically located on the flanks of villi
• increase in the number of Olfm4+ stem cells after tamoxifen treatment
• increased number after tamoxifen treatment
• form within 1 month of clonal deletion induced by low dose tamoxifen treatment
• contain Olfm4+ stem cells and Paneth cells

tumorigenesis
• form within 1 month of clonal deletion induced by low dose tamoxifen treatment
• contain Olfm4+ stem cells and Paneth cells

cellular
• following tamoxifen treatment a marked expansion of the proliferative compartment is seen

endocrine/exocrine glands
• following tamoxifen treatment a marked expansion of the proliferative compartment is seen with enlarged crypts and Ki67+ cells ectopically located on the flanks of villi
• increase in the number of Olfm4+ stem cells after tamoxifen treatment
• increased number after tamoxifen treatment




Genotype
MGI:5441534
cx36
Allelic
Composition
Xbp1tm3Glm/Xbp1tm3Glm
Tg(Vil-cre/ERT2)23Syr/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Vil-cre/ERT2)23Syr mutation (0 available)
Xbp1tm3Glm mutation (0 available); any Xbp1 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• reduced numbers in tamoxifen-treated mice
• in tamoxifen-treated mice
• increased apoptosis at the base of crypts (Paneth cells) and in villous epithelium (goblet cells) in tamoxifen-treated mice
• focal enteritis in 4 of 9 tamoxifen-treated mice ranges in severity from lamina propria polymorphpnuclear infiltration to crypt abscesses and ulceration without granulomas
• enteritis in 7 of 18 tamoxifen-treated mice

immune system
• focal enteritis in 4 of 9 tamoxifen-treated mice ranges in severity from lamina propria polymorphpnuclear infiltration to crypt abscesses and ulceration without granulomas
• enteritis in 7 of 18 tamoxifen-treated mice

cellular
• at the base of crypts (Paneth cells) and in villous epithelium (goblet cells) in tamoxifen-treated mice

endocrine/exocrine glands
• reduced numbers in tamoxifen-treated mice





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last database update
04/19/2016
MGI 6.03
The Jackson Laboratory