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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Vil1-cre)20Syr
transgene insertion 20, Sylvie Robine
MGI:3053819
Summary 45 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Epas1tm1Yms/Epas1tm1Yms
Tg(Vil1-cre)20Syr/0
B6.Cg-Epas1tm1Yms Tg(Vil1-cre)20Syr MGI:5446038
cn2
H2az1tm1.1Hko/H2az1tm1.1Hko
H2az2tm1.1Hko/H2az2tm1.1Hko
Tg(Vil1-cre)20Syr/0
B6.Cg-H2az1tm1.1Hko H2az2tm1.1Hko Tg(Vil1-cre)20Syr MGI:6360248
cn3
Abcb7tm1Mdf/Y
Tg(Vil1-cre)20Syr/0
either: (involves: 129S4/SvJae * C57BL/6 * DBA/2) or (involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2) MGI:3629063
cn4
Abcb7tm1Mdf/Abcb7+
Tg(Vil1-cre)20Syr/0
either: (involves: 129S4/SvJae * C57BL/6 * DBA/2) or (involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2) MGI:3629064
cn5
Cdh1tm1.1Mpst/Cdh1tm2Kem
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Tg(Vil1-cre)20Syr/0
involves: 129 * C57BL/6 * DBA/2 MGI:4822000
cn6
Cdh1tm2Kem/Cdh1+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Vil1-cre)20Syr/0
involves: 129 * C57BL/6 * DBA/2 MGI:5634401
cn7
Bmi1tm1.1Lees/Bmi1tm1.1Lees
Apctm2Cip/Apc+
Tg(Vil1-cre)20Syr/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2 MGI:5532577
cn8
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Vil1-cre)20Syr/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5634402
cn9
Bmi1tm1Brn/Bmi1tm1Brn
Apctm2Cip/Apc+
Cdkn2atm1Cjs/Cdkn2atm1Cjs
Tg(Vil1-cre)20Syr/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * DBA/2 MGI:5532576
cn10
Bmi1tm1Brn/Bmi1tm1Brn
Apctm2Cip/Apc+
Tg(Vil1-cre)20Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:5532574
cn11
Nf2tm2Gth/Nf2tm2Gth
Tg(Vil1-cre)20Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:3850478
cn12
Apctm2.1Cip/Apc+
Tg(Vil1-cre)20Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:4461183
cn13
Mbd3tm2Bh/Mbd3tm2Bh
Tg(Vil1-cre)20Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:4887392
cn14
Pikfyvetm2.1Tssk/Pikfyvetm2.1Tssk
Tg(Vil1-cre)20Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:5474983
cn15
E2f4tm2.1Lees/E2f4tm2.1Lees
E2f5tm1Dli/E2f5+
Tg(Vil1-cre)20Syr/0
involves: 129S1/Sv * 129S4/SvJae * C57BL/6 * DBA/2 MGI:5706798
cn16
Lrp5tm1Kry/Lrp5tm1Kry
Tph1tm1Kry/Tph1+
Tg(Vil1-cre)20Syr/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:3837415
cn17
Clcn3tm1Tjj/Clcn3tm1Tjj
Clcn5tm6.1Tjj/Y
Tg(Vil1-cre)20Syr/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:4834499
cn18
Neurog3tm3.1Ggr/Neurog3tm3.1Ggr
Tg(Vil1-cre)20Syr/0
involves: 129S2/SvPas * C57BL/6 * CD-1 * DBA/2 * SJL MGI:4460261
cn19
Neurog3tm1Fgu/Neurog3tm3.1Ggr
Tg(Vil1-cre)20Syr/0
involves: 129S2/SvPas * C57BL/6 * CD-1 * DBA/2 * SJL MGI:4460260
cn20
Htr1btm1Rhn/Htr1b+
Tph1tm1Kry/Tph1+
Tg(Vil1-cre)20Syr/0
involves: 129S2/SvPas * C57BL/6 * DBA/2 MGI:3837413
cn21
Gt(ROSA)26Sortm2(Rnf187)Jhai/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Vil1-cre)20Syr/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5013409
cn22
Slc40a1tm2Nca/Slc40a1tm2Nca
Tg(Vil1-cre)20Syr/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:3771552
cn23
Gt(ROSA)26Sortm1(Tfrc*)Nca/Gt(ROSA)26Sor+
Tfrctm3.1Nca/Tfrctm3.1Nca
Tg(Vil1-cre)20Syr/0
involves: 129S4/SvJae * C57BL/6 * CD-1 * DBA/2 MGI:5689324
cn24
Tfrctm3.1Nca/Tfrctm3.1Nca
Tg(Vil1-cre)20Syr/0
involves: 129S4/SvJae * C57BL/6 * CD-1 * DBA/2 MGI:5689322
cn25
E2f4tm2.1Lees/E2f4tm2.1Lees
Tg(Vil1-cre)20Syr/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5706796
cn26
Slc11a2tm2Nca/Slc11a2tm2Nca
Tg(Vil1-cre)20Syr/?
involves: 129S6.129S4-Slc11a2tm2Nca * C57BL/6 * DBA/2 MGI:3578660
cn27
ApcMin/Apc+
Gt(ROSA)26Sortm2(Rnf187)Jhai/Gt(ROSA)26Sor+
Tg(Vil1-cre)20Syr/0
involves: 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5013408
cn28
Msh2tm1Rak/Msh2tm2.1Rak
Tg(Vil1-cre)20Syr/0
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * DBA/2 * SJL MGI:4460268
cn29
Clcn4tm1Tjj/Clcn4tm1Tjj
Clcn5tm6.1Tjj/Y
Tg(Vil1-cre)20Syr/0
involves: 129/Sv * C57BL/6 * DBA/2 MGI:4834500
cn30
Msh2tm2.1Rak/Msh2tm3.1Rak
Tg(Vil1-cre)20Syr/0
involves: 129/Sv * C57BL/6 * DBA/2 * SJL MGI:4460267
cn31
Msh2tm2.1Rak/Msh2tm2.1Rak
Tg(Vil1-cre)20Syr/0
involves: 129/Sv * C57BL/6 * FVB/N * SJL MGI:4460266
cn32
Arnttm1.1Gonz/Arnttm1.1Gonz
Tg(Vil1-cre)20Syr/0
involves: 129X1/SvJ * C57BL/6 * DBA/2 MGI:5446037
cn33
St18tm1c(KOMP)Wtsi/St18tm1c(KOMP)Wtsi
Tg(Vil1-cre)20Syr/0
involves: C57BL/6 * C57BL/6N * DBA/2 MGI:6489912
cn34
Cdhr2tm1c(EUCOMM)Hmgu/Cdhr2tm1c(EUCOMM)Hmgu
Tg(Vil1-cre)20Syr/0
involves: C57BL/6 * C57BL/6N * DBA/2 MGI:6363536
cn35
Apctm1Tyj/Apc+
Tg(Vil1-cre)20Syr/0
involves: C57BL/6 * DBA/2 MGI:4461182
cn36
Tg(Vil1-cre)20Syr/0
Vmp1tm1.1Arte/Vmp1tm1.1Arte
involves: C57BL/6 * DBA/2 MGI:6386823
cn37
Tph1tm1Kry/Tph1tm1Kry
Tg(Vil1-cre)20Syr/0
involves: C57BL/6 * DBA/2 MGI:3837407
cn38
Lrp5tm3(Lrp5*)Kry/Lrp5tm3(Lrp5*)Kry
Tg(Vil1-cre)20Syr/0
involves: C57BL/6 * DBA/2 MGI:3837405
cn39
Lrp5tm2Kry/Lrp5+
Tg(Vil1-cre)20Syr/0
involves: C57BL/6 * DBA/2 MGI:3837404
cn40
Lrp5tm2Kry/Lrp5tm2Kry
Tg(Vil1-cre)20Syr/0
involves: C57BL/6 * DBA/2 MGI:3837403
cn41
Znhit1tm1.1Nju/Znhit1tm1.1Nju
Tg(Vil1-cre)20Syr/0
involves: C57BL/6 * DBA/2 MGI:6360245
cn42
Nrastm1Tyj/Nras+
Tg(Vil1-cre)20Syr/0
involves: C57BL/6 * DBA/2 MGI:3776027
cn43
Gt(ROSA)26Sortm2(sb11)Njen/Gt(ROSA)26Sor+
Tg(Vil1-cre)20Syr/0
TgTn(sb-T2/Onc)68Dla/0
involves: C57BL/6 * DBA/2 * FVB/N MGI:3839797
cn44
Gt(ROSA)26Sortm2(sb11)Njen/Gt(ROSA)26Sor+
Tg(Vil1-cre)20Syr/0
TgTn(sb-T2/Onc)76Dla/0
involves: C57BL/6 * DBA/2 * FVB/N MGI:3839798
cn45
Cep55tm1c(EUCOMM)Hmgu/Cep55tm1c(EUCOMM)Hmgu
Tg(Vil1-cre)20Syr/0
involves: C57BL/6N * DBA/2 MGI:6458516


Genotype
MGI:5446038
cn1
Allelic
Composition
Epas1tm1Yms/Epas1tm1Yms
Tg(Vil1-cre)20Syr/0
Genetic
Background
B6.Cg-Epas1tm1Yms Tg(Vil1-cre)20Syr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Epas1tm1Yms mutation (0 available); any Epas1 mutation (47 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system

homeostasis/metabolism




Genotype
MGI:6360248
cn2
Allelic
Composition
H2az1tm1.1Hko/H2az1tm1.1Hko
H2az2tm1.1Hko/H2az2tm1.1Hko
Tg(Vil1-cre)20Syr/0
Genetic
Background
B6.Cg-H2az1tm1.1Hko H2az2tm1.1Hko Tg(Vil1-cre)20Syr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2az1tm1.1Hko mutation (0 available); any H2az1 mutation (19 available)
H2az2tm1.1Hko mutation (0 available); any H2az2 mutation (20 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body

digestive/alimentary system
• crypt cells fail to form intestinal organoids in vitro

endocrine/exocrine glands
• crypt cells fail to form intestinal organoids in vitro




Genotype
MGI:3629063
cn3
Allelic
Composition
Abcb7tm1Mdf/Y
Tg(Vil1-cre)20Syr/0
Genetic
Background
either: (involves: 129S4/SvJae * C57BL/6 * DBA/2) or (involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abcb7tm1Mdf mutation (1 available); any Abcb7 mutation (6 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging




Genotype
MGI:3629064
cn4
Allelic
Composition
Abcb7tm1Mdf/Abcb7+
Tg(Vil1-cre)20Syr/0
Genetic
Background
either: (involves: 129S4/SvJae * C57BL/6 * DBA/2) or (involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abcb7tm1Mdf mutation (1 available); any Abcb7 mutation (6 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging




Genotype
MGI:4822000
cn5
Allelic
Composition
Cdh1tm1.1Mpst/Cdh1tm2Kem
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh1tm1.1Mpst mutation (0 available); any Cdh1 mutation (120 available)
Cdh1tm2Kem mutation (1 available); any Cdh1 mutation (120 available)
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (556 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype




Genotype
MGI:5634401
cn6
Allelic
Composition
Cdh1tm2Kem/Cdh1+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh1tm2Kem mutation (1 available); any Cdh1 mutation (120 available)
Smad4tm2.1Cxd mutation (2 available); any Smad4 mutation (32 available)
Tg(Vil1-cre)20Syr mutation (3 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (157 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice develop intestinal adenocarcinomas with a median tumor-free survival of 5.2 months of age and no distant metastases are seen

neoplasm
• mice develop intestinal adenocarcinomas with a median tumor-free survival of 5.2 months of age and no distant metastases are seen




Genotype
MGI:5532577
cn7
Allelic
Composition
Bmi1tm1.1Lees/Bmi1tm1.1Lees
Apctm2Cip/Apc+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2Cip mutation (0 available); any Apc mutation (59 available)
Bmi1tm1.1Lees mutation (1 available); any Bmi1 mutation (6 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• reduced visible and total lesions in the small intestine

digestive/alimentary system
• reduced visible and total lesions in the small intestine

cellular
N
• no increase in apoptosis is observed in non tumor tissue




Genotype
MGI:5634402
cn8
Allelic
Composition
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smad4tm2.1Cxd mutation (2 available); any Smad4 mutation (32 available)
Tg(Vil1-cre)20Syr mutation (3 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (157 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice develop intestinal adenocarcinomas with a median tumor-free survival of 5.4 months of age and no distant metastases are seen

neoplasm
• mice develop intestinal adenocarcinomas with a median tumor-free survival of 5.4 months of age and no distant metastases are seen




Genotype
MGI:5532576
cn9
Allelic
Composition
Bmi1tm1Brn/Bmi1tm1Brn
Apctm2Cip/Apc+
Cdkn2atm1Cjs/Cdkn2atm1Cjs
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2Cip mutation (0 available); any Apc mutation (59 available)
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (6 available)
Cdkn2atm1Cjs mutation (6 available); any Cdkn2a mutation (51 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• increased size and number of small intestine adenomas

growth/size/body
• found in some animals by 90 days of age

behavior/neurological
• hunching appears in some animals at 90 days of age

neoplasm
• increased size and number of small intestine adenomas




Genotype
MGI:5532574
cn10
Allelic
Composition
Bmi1tm1Brn/Bmi1tm1Brn
Apctm2Cip/Apc+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2Cip mutation (0 available); any Apc mutation (59 available)
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (6 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• tumors in small intestine are almost absent at 120 days of age
• fewer and smaller tumors at 90 days of age as well
• decrease in numbers of tumors between 90 and 120 days
• no increase in tumor size between 90 and 120 days
• also reduced at 120 days
• adenomas are one tenth the size of those found in controls at 120 days of age
• increased cell proliferation in adenomas at 90 days
• increased apoptosis in smaller adenomas but not larger ones at 90 days
• apoptosis is also increased in non tumor tissue

neoplasm
• tumors in small intestine are almost absent at 120 days of age
• fewer and smaller tumors at 90 days of age as well
• decrease in numbers of tumors between 90 and 120 days
• no increase in tumor size between 90 and 120 days
• also reduced at 120 days
• adenomas are one tenth the size of those found in controls at 120 days of age
• increased cell proliferation in adenomas at 90 days
• increased apoptosis in smaller adenomas but not larger ones at 90 days
• apoptosis is also increased in non tumor tissue

cellular
• increased apoptosis in smaller adenomas but not larger ones at 90 days
• apoptosis is also increased in non tumor tissue




Genotype
MGI:3850478
cn11
Allelic
Composition
Nf2tm2Gth/Nf2tm2Gth
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf2tm2Gth mutation (3 available); any Nf2 mutation (67 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• lesions in the renal tubule epithelia are observed as early as 15 days of age with most initiating in the corticomedullary junctions as projections of atypical epithelial cells into the proximal convoluted tubule lumen
• by 3 months of age, all mice develop lumen-filling intratubular neoplasia unlike wild-type mice
• by 6 months, tumors increase in size and number penetrating tubule basement membrane as invasive carcinomas
• renal tubule carcinoma cells exhibit a 7-fold increase in proliferation compared to in Nf2tm2Gth homozygotes
• however, treatment with erlotinib reduces cell proliferation

mortality/aging
• mice die by 10 months of age
• mice occasionally die between E17 and P3
• mice occasionally die between E17 and P3
• fewer than expected mice survive until weaning

neoplasm
• lesions in the renal tubule epithelia are observed as early as 15 days of age with most initiating in the corticomedullary junctions as projections of atypical epithelial cells into the proximal convoluted tubule lumen
• by 3 months of age, all mice develop lumen-filling intratubular neoplasia unlike wild-type mice
• by 6 months, tumors increase in size and number penetrating tubule basement membrane as invasive carcinomas
• renal tubule carcinoma cells exhibit a 7-fold increase in proliferation compared to in Nf2tm2Gth homozygotes
• however, treatment with erlotinib reduces cell proliferation

growth/size/body

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
renal cell carcinoma DOID:4450 OMIM:300854
J:150071




Genotype
MGI:4461183
cn12
Allelic
Composition
Apctm2.1Cip/Apc+
Tg(Vil1-cre)20Syr/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 (59 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:4887392
cn13
Allelic
Composition
Mbd3tm2Bh/Mbd3tm2Bh
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mbd3tm2Bh mutation (2 available); any Mbd3 mutation (54 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• increase in intestinal progenitor cell proliferation in the crypts
• large increase in proliferating cells compared to controls following DSS treatment

neoplasm
• striking increase in the number of tumors in mice following azoxymethane and DSS treatment
• tumors induced by azoxymethane and DSS treatment are increased in size compared to controls

homeostasis/metabolism
• striking increase in the number of tumors in mice following azoxymethane and DSS treatment

immune system
• large increase in proliferating cells compared to controls following DSS treatment

cellular
• increase in intestinal progenitor cell proliferation in the crypts




Genotype
MGI:5474983
cn14
Allelic
Composition
Pikfyvetm2.1Tssk/Pikfyvetm2.1Tssk
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pikfyvetm2.1Tssk mutation (0 available); any Pikfyve mutation (5 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• only 20% of mice born alive survive beyond 100 days
• only 20% of mice born alive survive beyond 100 days
• recovered at a lower than expected Mendelian frequency

digestive/alimentary system
• enterocytes expressing cre have enlarged endosomes
• marked vacuolation of enterocytes in the ileum
• decrease in actin at the apical surface and ectopic localization of DPP4 and IAP
• overt fibrosis of the muscularis mucosa
• lymphocyte infiltration is prominent in both the mucosa and submucosa

homeostasis/metabolism
• decrease in circulating choline esterase levels

growth/size/body
• at 5 weeks of age, average weight is about 60% of the mean littermate control body weight

behavior/neurological

integument

immune system
• lymphocyte infiltration is prominent in both the mucosa and submucosa

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Crohn's disease DOID:8778 J:193689




Genotype
MGI:5706798
cn15
Allelic
Composition
E2f4tm2.1Lees/E2f4tm2.1Lees
E2f5tm1Dli/E2f5+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
E2f4tm2.1Lees mutation (1 available); any E2f4 mutation (14 available)
E2f5tm1Dli mutation (1 available); any E2f5 mutation (2 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
N
• male mice exhibit normal spermatogenesis
• often contains many spermatozoa
• with dilation at that the expense of the epithelium
• spermatozoa accumulate in the efferent ducts unlike in wild-type mice
• efferent duct epithelium lacks multiciliated cells and exhibit decreased abundance of endocytic vesicle apparatus
• no spermatozoa are detected in the epididymis

endocrine/exocrine glands
• often contains many spermatozoa
• with dilation at that the expense of the epithelium




Genotype
MGI:3837415
cn16
Allelic
Composition
Lrp5tm1Kry/Lrp5tm1Kry
Tph1tm1Kry/Tph1+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lrp5tm1Kry mutation (0 available); any Lrp5 mutation (51 available)
Tg(Vil1-cre)20Syr mutation (3 available)
Tph1tm1Kry mutation (0 available); any Tph1 mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
N
• loss of expression of 1 copy of Tph1 in the gut rescues the bone phenotype seen in Lrp5 null mice




Genotype
MGI:4834499
cn17
Allelic
Composition
Clcn3tm1Tjj/Clcn3tm1Tjj
Clcn5tm6.1Tjj/Y
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Clcn3tm1Tjj mutation (0 available); any Clcn3 mutation (97 available)
Clcn5tm6.1Tjj mutation (0 available); any Clcn5 mutation (13 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• mice exhibit reduced endocytic uptake of beta-lactoglobulin by proximal tubule cells similar to in Clcn5tm1Tjj homozygotes

homeostasis/metabolism
• mice exhibit reduced endocytic uptake of beta-lactoglobulin by proximal tubule cells similar to in Clcn5tm1Tjj homozygotes




Genotype
MGI:4460261
cn18
Allelic
Composition
Neurog3tm3.1Ggr/Neurog3tm3.1Ggr
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * CD-1 * DBA/2 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Neurog3tm3.1Ggr mutation (0 available); any Neurog3 mutation (15 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Loss of enteroendocrine cells in Neurog3tm1Fgu/Neurog3tm3.1Ggr Tg(Vil1-cre)20Syr/0 and Neurog3tm3.1Ggr/Neurog3tm3.1Ggr Tg(Vil1-cre)20Syr/0 mice

mortality/aging
• 50% of mice die within the first 8 days of life

homeostasis/metabolism
• mice excrete yellowish stool unlike wild-type mice
• in an intraperitoneal glucose tolerance test, mice exhibit lower serum glucose levels than in similarly treated wild-type mice
• fasting mice exhibit decreased blood glucose compared with similarly treated wild-type mice
• in an oral glucose tolerance test, mice exhibit improved glucose clearance compared with similarly treated wild-type mice
• in an intraperitoneal glucose tolerance test, mice exhibit lower serum glucose levels than in similarly treated wild-type mice
• slightly at 14 and 17 weeks
• insulin-mediated hypoglycemic response is blunted compared to in wild-type mice

digestive/alimentary system
• goblet cells in the large intestine are larger than in wild-type mice and mostly devoid of mucus
• however, goblet cell numbers are normal in the small intestine
• at E19.5, crypt cell proliferation is increased compared to in wild-type mice
• in adult mice, crypt cell proliferation is increased with an up to 1.6-fold increase in cell turnover compared to in wild-type mice
• as early as embryogenesis, mice lack enteroendocrine progenitors along the proximal-distal axis of the intestine unlike in wild-type mice
• however, intestinal epithelial cell proliferation is normal
• as early as embryogenesis, mice lack enteroendocrine progenitors along the proximal-distal axis of the intestine unlike in wild-type mice
• small intestine crypts are disorganized, larger, and more abundant than in wild-type mice
• the large intestine exhibits a reduction in the length of glands of up to 1.5 times compared with wild-type mice
• villi are blunted or club shaped with frequent dilation and strong detachment of the epithelium from the basement membrane unlike in wild-type mice
• microvilli on absorptive cells are sparser, 60% shorter, but twice as large as on wild-type cells
• the brush border of absorptive cells in the small intestine is reduced 44% compared to in wild-type mice
• however, expression of brush border enzymes and glucose transporters is normal
• 60% shorter than in wild-type mice
• mice produce more feces compared with wild-type mice
• surviving mice exhibit soft stool that does not cease with age unlike in wild-type mice
• mice excrete yellowish stool unlike wild-type mice
• intestinal transit time is increased 2.3-fold compared to in wild-type mice

growth/size/body

adipose tissue
• mice exhibit reduced abdominal fat compared with wild-type mice

endocrine/exocrine glands
• small intestine crypts are disorganized, larger, and more abundant than in wild-type mice
• mice exhibit more medium and large islets with centrally located alpha cells than in wild-type mice
• mice exhibit a shift from large to single islets compared with wild-type mice

cellular
• goblet cells in the large intestine are larger than in wild-type mice and mostly devoid of mucus
• however, goblet cell numbers are normal in the small intestine
• at E19.5, crypt cell proliferation is increased compared to in wild-type mice
• in adult mice, crypt cell proliferation is increased with an up to 1.6-fold increase in cell turnover compared to in wild-type mice




Genotype
MGI:4460260
cn19
Allelic
Composition
Neurog3tm1Fgu/Neurog3tm3.1Ggr
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * CD-1 * DBA/2 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Neurog3tm1Fgu mutation (0 available); any Neurog3 mutation (15 available)
Neurog3tm3.1Ggr mutation (0 available); any Neurog3 mutation (15 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Loss of enteroendocrine cells in Neurog3tm1Fgu/Neurog3tm3.1Ggr Tg(Vil1-cre)20Syr/0 and Neurog3tm3.1Ggr/Neurog3tm3.1Ggr Tg(Vil1-cre)20Syr/0 mice

mortality/aging
• 50% of mice die within the first 8 days of life

digestive/alimentary system
• goblet cells in the large intestine are larger than in wild-type mice and mostly devoid of mucus
• however, goblet cell numbers are normal in the small intestine
• at E19.5, crypt cell proliferation is increased compared to in wild-type mice
• in adult mice, crypt cell proliferation is increased with an up to 1.6-fold increase in cell turnover compared to in wild-type mice
• as early as embryogenesis, mice lack enteroendocrine progenitors along the proximal-distal axis of the intestine unlike in wild-type mice
• however, intestinal epithelial cell proliferation is normal
• as early as embryogenesis, mice lack enteroendocrine progenitors along the proximal-distal axis of the intestine unlike in wild-type mice
• small intestine crypts are disorganized, larger, and more abundant than in wild-type mice
• the large intestine exhibits a reduction in the length of glands of up to 1.5 times compared with wild-type mice
• villi are blunted or club shaped with frequent dilation and strong detachment of the epithelium from the basement membrane unlike in wild-type mice
• microvilli on absorptive cells are sparser, 60% shorter, but twice as large as on wild-type cells
• the brush border of absorptive cells in the small intestine is reduced 44% compared to in wild-type mice
• however, expression of brush border enzymes and glucose transporters is normal
• 60% shorter than in wild-type mice
• mice produce more feces compared with wild-type mice
• surviving mice exhibit soft stool that does not cease with age unlike in wild-type mice
• mice excrete yellowish stool unlike wild-type mice
• intestinal transit time is increased 2.3-fold compared to in wild-type mice

homeostasis/metabolism
• mice excrete yellowish stool unlike wild-type mice
• in an intraperitoneal glucose tolerance test, mice exhibit lower serum glucose levels than in similarly treated wild-type mice
• fasting mice exhibit decreased blood glucose compared with similarly treated wild-type mice
• in an oral glucose tolerance test, mice exhibit improved glucose clearance compared with similarly treated wild-type mice
• in an intraperitoneal glucose tolerance test, mice exhibit lower serum glucose levels than in similarly treated wild-type mice
• slightly at 14 and 17 weeks
• insulin-mediated hypoglycemic response is blunted compared to in wild-type mice

growth/size/body

adipose tissue
• mice exhibit reduced abdominal fat compared with wild-type mice

endocrine/exocrine glands
• small intestine crypts are disorganized, larger, and more abundant than in wild-type mice
• mice exhibit more medium and large islets with centrally located alpha cells than in wild-type mice
• mice exhibit a shift from large to single islets compared with wild-type mice

cellular
• goblet cells in the large intestine are larger than in wild-type mice and mostly devoid of mucus
• however, goblet cell numbers are normal in the small intestine
• at E19.5, crypt cell proliferation is increased compared to in wild-type mice
• in adult mice, crypt cell proliferation is increased with an up to 1.6-fold increase in cell turnover compared to in wild-type mice




Genotype
MGI:3837413
cn20
Allelic
Composition
Htr1btm1Rhn/Htr1b+
Tph1tm1Kry/Tph1+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Htr1btm1Rhn mutation (3 available); any Htr1b mutation (17 available)
Tg(Vil1-cre)20Syr mutation (3 available)
Tph1tm1Kry mutation (0 available); any Tph1 mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• phenotype is the same as in mice homozygous null for Htr1b and mice conditional null for Tph1 in the gut




Genotype
MGI:5013409
cn21
Allelic
Composition
Gt(ROSA)26Sortm2(Rnf187)Jhai/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(Rnf187)Jhai mutation (0 available); any Gt(ROSA)26Sor mutation (556 available)
Krastm4Tyj mutation (9 available); any Kras mutation (38 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice exhibit increased cell proliferation in the colonic crypt compared with wild-type mice

cellular
• mice exhibit increased cell proliferation in the colonic crypt compared with wild-type mice




Genotype
MGI:3771552
cn22
Allelic
Composition
Slc40a1tm2Nca/Slc40a1tm2Nca
Tg(Vil1-cre)20Syr/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 (28 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no mice are found at birth due to recombination in the extraembryonic visceral endoderm




Genotype
MGI:5689324
cn23
Allelic
Composition
Gt(ROSA)26Sortm1(Tfrc*)Nca/Gt(ROSA)26Sor+
Tfrctm3.1Nca/Tfrctm3.1Nca
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CD-1 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Tfrc*)Nca mutation (1 available); any Gt(ROSA)26Sor mutation (556 available)
Tfrctm3.1Nca mutation (2 available); any Tfrc mutation (22 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• some mice die postnatally
• however, most mice are alive at 2 months

digestive/alimentary system
• mice that die exhibit the same phenotype as Tfrctm3.1Nca/Tfrctm3.1Nca Tg(Vil-cre)20Syr mice
• however, mice that survive at 2 months exhibit normal architecture and proliferation of crypt intestinal epithelial cells




Genotype
MGI:5689322
cn24
Allelic
Composition
Tfrctm3.1Nca/Tfrctm3.1Nca
Tg(Vil1-cre)20Syr/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 (22 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die before P3 with variable timing
• treatment with iron dextran does not extend lifespan

digestive/alimentary system
• reduced proliferation in intervillous regions
• mice exhibit milk in intestinal lumen, shorter intestines with apparent melena compared with wild-type mice
• larger intestinal epithelial cells contain vacuole-like lipid accumulation than in wild-type cells
• severe disruption of epithelial integrity with blunted villi, smaller intervillous regions, edema in the lamina propria and enlarged vacuole-like structures in the intestinal epithelial cells at P2
• reduced length with apparent melena
• severe disruption of epithelial integrity with blunted villi, smaller intervillous regions, edema in the lamina propria and enlarged vacuole-like structures in the intestinal epithelial cells at E18.5 and P2
• severe disruption of epithelial integrity with blunted villi, smaller intervillous regions, edema in the lamina propria and enlarged vacuole-like structures in the intestinal epithelial cells at P2
• with milk

growth/size/body
• mice fail to thrice and are runted by P1

cellular
• reduced proliferation in intervillous regions




Genotype
MGI:5706796
cn25
Allelic
Composition
E2f4tm2.1Lees/E2f4tm2.1Lees
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
E2f4tm2.1Lees mutation (1 available); any E2f4 mutation (14 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice are viable and fertile with normal intestinal morphology and efferent duct epithelium




Genotype
MGI:3578660
cn26
Allelic
Composition
Slc11a2tm2Nca/Slc11a2tm2Nca
Tg(Vil1-cre)20Syr/?
Genetic
Background
involves: 129S6.129S4-Slc11a2tm2Nca * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc11a2tm2Nca mutation (1 available); any Slc11a2 mutation (13 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body

hematopoietic system
• sinusoid areas of the liver particularly
• dysplastic erythropoiesis in the spleen
• progressive anemia developed after birth
• profound but not as severe as in knock-out mice
• decreased non-heme iron in the spleen
• expanded red pulp

homeostasis/metabolism
• decreased non-heme iron in the heart
• decreased non-heme iron in the spleen
• diminished non-heme iron levels in the brain
• decreased non-heme iron
• decreased non-heme iron in the liver

cardiovascular system
• decreased non-heme iron in the heart

immune system
• decreased non-heme iron in the spleen
• expanded red pulp

liver/biliary system
• decreased non-heme iron in the liver

renal/urinary system
• decreased non-heme iron

nervous system
• diminished non-heme iron levels in the brain




Genotype
MGI:5013408
cn27
Allelic
Composition
ApcMin/Apc+
Gt(ROSA)26Sortm2(Rnf187)Jhai/Gt(ROSA)26Sor+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (12 available); any Apc mutation (59 available)
Gt(ROSA)26Sortm2(Rnf187)Jhai mutation (0 available); any Gt(ROSA)26Sor mutation (556 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• intestinal tumors are increased in number compared to in ApcMin/Apc+ Tg(Vil-cre)20Syr

neoplasm
• intestinal tumors are increased in number compared to in ApcMin/Apc+ Tg(Vil-cre)20Syr
• intestinal tumors exhibit increased cell proliferation and size compared to in ApcMin/Apc+ Tg(Vil-cre)20Syr




Genotype
MGI:4460268
cn28
Allelic
Composition
Msh2tm1Rak/Msh2tm2.1Rak
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * DBA/2 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Msh2tm1Rak mutation (1 available); any Msh2 mutation (36 available)
Msh2tm2.1Rak mutation (1 available); any Msh2 mutation (36 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• beginning at 6 months, mice develop intestinal tumors
• by 10 months, 50% of mice develop intestinal tumors

neoplasm
• beginning at 6 months, mice develop intestinal tumors
• by 10 months, 50% of mice develop intestinal tumors
• mice develop fewer and larger tumors than in Msh2tm2.1Rak/Msh2tm3.1Wed Tg(Vil-cre)20Syr mice
• tumors do not respond to treatment with cisplatin or FOLFOX unlike tumors from Msh2tm2.1Rak/Msh2tm3.1Wed Tg(Vil-cre)20Syr mice

homeostasis/metabolism
• tumor cells exhibit increased microsatellite instability compared with wild-type cells
• tumors do not respond to treatment with cisplatin or FOLFOX unlike tumors from Msh2tm2.1Rak/Msh2tm3.1Wed Tg(Vil-cre)20Syr mice
• FOLFOX-treated intestinal mucosa exhibit decreased apoptosis compared with similarly treated cells from Msh2tm2.1Wed homozygotes and Msh2tm2.1Rak/Msh2tm3.1Wed Tg(Vil-cre)20Syr mice

cellular
• tumor cells exhibit increased microsatellite instability compared with wild-type cells

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Lynch syndrome DOID:3883 OMIM:PS120435
J:161577




Genotype
MGI:4834500
cn29
Allelic
Composition
Clcn4tm1Tjj/Clcn4tm1Tjj
Clcn5tm6.1Tjj/Y
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129/Sv * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Clcn4tm1Tjj mutation (0 available); any Clcn4 mutation (37 available)
Clcn5tm6.1Tjj mutation (0 available); any Clcn5 mutation (13 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• mice exhibit reduced endocytic uptake of beta-lactoglobulin by proximal tubule cells similar to in Clcn5tm1Tjj homozygotes

homeostasis/metabolism
• mice exhibit reduced endocytic uptake of beta-lactoglobulin by proximal tubule cells similar to in Clcn5tm1Tjj homozygotes




Genotype
MGI:4460267
cn30
Allelic
Composition
Msh2tm2.1Rak/Msh2tm3.1Rak
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129/Sv * C57BL/6 * DBA/2 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Msh2tm2.1Rak mutation (1 available); any Msh2 mutation (36 available)
Msh2tm3.1Rak mutation (0 available); any Msh2 mutation (36 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• beginning at 10 months, mice develop intestinal tumors
• by 13 months, 50% of mice develop intestinal tumors

neoplasm
• beginning at 10 months, mice develop intestinal tumors
• by 13 months, 50% of mice develop intestinal tumors
• mice develop more and smaller tumors than in Msh2tm1Rak/Msh2tm2.1Wed Tg(Vil-cre)20Syr mice
• tumors respond to treatment with cisplatin or FOLFOX unlike tumors from Msh2tm1Rak/Msh2tm2.1Wed Tg(Vil-cre)20Syr mice

homeostasis/metabolism
• tumor cells exhibit increased microsatellite instability compared with wild-type cells
• tumors respond to treatment with cisplatin or FOLFOX unlike tumors from Msh2tm1Rak/Msh2tm2.1Wed Tg(Vil-cre)20Syr mice
• FOLFOX-treated intestinal mucosa cells exhibit decreased apoptosis compared with similarly treated cells from Msh2tm2.1Wed homozygotes but increased compared with similarly treated cell from Msh2tm1Rak/Msh2tm2.1Wed Tg(Vil-cre)20Syr mice

cellular
• tumor cells exhibit increased microsatellite instability compared with wild-type cells

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Lynch syndrome DOID:3883 OMIM:PS120435
J:161577




Genotype
MGI:4460266
cn31
Allelic
Composition
Msh2tm2.1Rak/Msh2tm2.1Rak
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129/Sv * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Msh2tm2.1Rak mutation (1 available); any Msh2 mutation (36 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 89% of mice develop small intestine tumors compared with 6% of wild-type mice
• 50% of small intestine tumors are adenomas while the rest are highly invasive adenocarcinomas
• 50% of small intestine tumors are highly invasive adenocarcinomas
• 50% of small intestine tumors are adenomas

mortality/aging
• all mice die by 17 months of age

neoplasm
• 89% of mice develop small intestine tumors compared with 6% of wild-type mice
• 50% of small intestine tumors are adenomas while the rest are highly invasive adenocarcinomas
• 50% of small intestine tumors are highly invasive adenocarcinomas
• 50% of small intestine tumors are adenomas
• in only 1 of 150 mice

homeostasis/metabolism
• intestinal epithelial cells exhibit an increase in microsatellite instability compared with wild-type cells
• tumor cells exhibit increased microsatellite instability compared with wild-type cells

cellular
• intestinal epithelial cells exhibit an increase in microsatellite instability compared with wild-type cells
• tumor cells exhibit increased microsatellite instability compared with wild-type cells

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Lynch syndrome DOID:3883 OMIM:PS120435
J:161577




Genotype
MGI:5446037
cn32
Allelic
Composition
Arnttm1.1Gonz/Arnttm1.1Gonz
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Arnttm1.1Gonz mutation (0 available); any Arnt mutation (15 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system

homeostasis/metabolism




Genotype
MGI:6489912
cn33
Allelic
Composition
St18tm1c(KOMP)Wtsi/St18tm1c(KOMP)Wtsi
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: C57BL/6 * C57BL/6N * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
St18tm1c(KOMP)Wtsi mutation (0 available); any St18 mutation (40 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
N
• normal susceptibility to weight loss after oral DSS administration

mortality/aging
N
• normal sensitivity to DSS-induced colitis (diarrhea, weight loss, intestinal inflammation, vascular leakage in intestines)




Genotype
MGI:6363536
cn34
Allelic
Composition
Cdhr2tm1c(EUCOMM)Hmgu/Cdhr2tm1c(EUCOMM)Hmgu
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: C57BL/6 * C57BL/6N * DBA/2
Cell Lines HEPD0749_5_F10
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdhr2tm1c(EUCOMM)Hmgu mutation (0 available); any Cdhr2 mutation (2 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• at P90, body weight is significantly lower than that of wild-type controls
• growth begins to lag behind that of wild-type controls in the second month of life into adulthood

digestive/alimentary system
• SEM analysis of the intestinal epithelium revealed bare regions that lack closely spaced villi
• villus surfaces appear rougher and less flat than those in wild-type controls
• enterocytes exhibit a domed apical surface with an abnormal outward/convex curvature
• however, apical-basolateral polarity and simple columnar morphology remain normal
• mean crypt depth at the proximal (duodenal) end of the small intestine is significantly decreased
• TEM of the brush borders in jejunal tissues revealed that enterocytes show prominent apical doming
• intermicrovillar adhesion complex (IMAC) components CDHR5, USH1C, and MYO7B are displaced from their normal localization at the tips of microvilli, unlike in wild-type controls
• microvilli are significantly shorter and more variable in length, and show a splayed morphology with significant physical separation and free space between neighboring protrusions
• intermicrovillar adhesion links, normally seen at the tips of wild-type microvilli, are almost entirely absent; in rare cases, remnant link-like structures between some microvilli are observed
• a subset of microvilli show irregular non-cylindrical shapes such that cross-sections show more angular or oblong profiles rather than circular and cross-sectional area is significantly increased
• misshapen microvilli have abnormally large, poorly consolidated core actin bundles or in some cases multiple core-like structures
• microvilli show a striking loss of hexagonal packing order and reduced packing density, with enterocytes having ~33% fewer protrusions per unit apical area relative to wild-type controls
• mean villus length at the proximal (duodenal) end of the small intestine is significantly decreased
• levels of key apical enzymes and transporters that are critical for enterocyte function are significantly reduced in the brush border

endocrine/exocrine glands
• mean crypt depth at the proximal (duodenal) end of the small intestine is significantly decreased




Genotype
MGI:4461182
cn35
Allelic
Composition
Apctm1Tyj/Apc+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Tyj mutation (1 available); any Apc mutation (59 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• develop several lesions in the small intestines and colons by 4 - 5 months of age
• develop by 4 - 5 months of age

neoplasm
• develop several lesions in the small intestines and colons by 4 - 5 months of age
• develop by 4 - 5 months of age




Genotype
MGI:6386823
cn36
Allelic
Composition
Tg(Vil1-cre)20Syr/0
Vmp1tm1.1Arte/Vmp1tm1.1Arte
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Vil1-cre)20Syr mutation (3 available)
Vmp1tm1.1Arte mutation (0 available); any Vmp1 mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• accumulation of neutral lipids in intestinal epithelia at 8 months of age

growth/size/body
• at 7 to 10 months of age

homeostasis/metabolism
• accumulation of neutral lipids in intestinal epithelia at 8 months of age
• however, serum cholesterol and lipoproteins levels are normal




Genotype
MGI:3837407
cn37
Allelic
Composition
Tph1tm1Kry/Tph1tm1Kry
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Vil1-cre)20Syr mutation (3 available)
Tph1tm1Kry mutation (0 available); any Tph1 mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• decreased circulating serotonin levels

cellular
• increased osteoblast proliferation

homeostasis/metabolism
• decreased circulating serotonin levels

skeleton
• increased osteoblast proliferation
• severe
• ovariectomy does not result in decreased bone mass unlike in controls
• increased bone formation




Genotype
MGI:3837405
cn38
Allelic
Composition
Lrp5tm3(Lrp5*)Kry/Lrp5tm3(Lrp5*)Kry
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lrp5tm3(Lrp5*)Kry mutation (0 available); any Lrp5 mutation (51 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• decreased circulating serotonin levels

nervous system
• decreased circulating serotonin levels

skeleton
• increased bone formation




Genotype
MGI:3837404
cn39
Allelic
Composition
Lrp5tm2Kry/Lrp5+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lrp5tm2Kry mutation (0 available); any Lrp5 mutation (51 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• decreased bone formation




Genotype
MGI:3837403
cn40
Allelic
Composition
Lrp5tm2Kry/Lrp5tm2Kry
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lrp5tm2Kry mutation (0 available); any Lrp5 mutation (51 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• circulating serotonin levels are 5- to 8-fold higher compared to controls

cellular
• decreased osteoblast proliferation

homeostasis/metabolism
• circulating serotonin levels are 5- to 8-fold higher compared to controls

skeleton
• decreased osteoblast proliferation
• decreased bone formation

vision/eye
N
• unlike in null mice, persistence of hyaloid vessels is not seen




Genotype
MGI:6360245
cn41
Allelic
Composition
Znhit1tm1.1Nju/Znhit1tm1.1Nju
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Vil1-cre)20Syr mutation (3 available)
Znhit1tm1.1Nju mutation (0 available); any Znhit1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• some mice die following the first week after birth

digestive/alimentary system
• enlarged postnatally that fail to form intestinal organoids in vitro
• however, embryonic intestinal development is normal

growth/size/body
• from P5 through P30

endocrine/exocrine glands
• enlarged postnatally that fail to form intestinal organoids in vitro
• however, embryonic intestinal development is normal




Genotype
MGI:3776027
cn42
Allelic
Composition
Nrastm1Tyj/Nras+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nrastm1Tyj mutation (1 available); any Nras mutation (23 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• one week after exposure to 2.5% dextran sodium sulfate (DSS), colonic epithelium shows high resistance to the effects relative to wild-type and Kras mutant animals; sensitivity to DSS-induced apoptosis is strongly reduced




Genotype
MGI:3839797
cn43
Allelic
Composition
Gt(ROSA)26Sortm2(sb11)Njen/Gt(ROSA)26Sor+
Tg(Vil1-cre)20Syr/0
TgTn(sb-T2/Onc)68Dla/0
Genetic
Background
involves: C57BL/6 * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(sb11)Njen mutation (7 available); any Gt(ROSA)26Sor mutation (556 available)
TgTn(sb-T2/Onc)68Dla mutation (1 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• increased incidence of intraepithelial neoplasias in the small and large intestines
• adenomas are seen in the small and large intestines

mortality/aging

neoplasm
• increased incidence of intraepithelial neoplasias in the small and large intestines
• adenomas are seen in the small and large intestines




Genotype
MGI:3839798
cn44
Allelic
Composition
Gt(ROSA)26Sortm2(sb11)Njen/Gt(ROSA)26Sor+
Tg(Vil1-cre)20Syr/0
TgTn(sb-T2/Onc)76Dla/0
Genetic
Background
involves: C57BL/6 * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(sb11)Njen mutation (7 available); any Gt(ROSA)26Sor mutation (556 available)
TgTn(sb-T2/Onc)76Dla mutation (1 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• increased incidence of intraepithelial neoplasias in the small and large intestines
• adenomas are seen in the small and large intestines

mortality/aging

neoplasm
• increased incidence of intraepithelial neoplasias in the small and large intestines
• adenomas are seen in the small and large intestines




Genotype
MGI:6458516
cn45
Allelic
Composition
Cep55tm1c(EUCOMM)Hmgu/Cep55tm1c(EUCOMM)Hmgu
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: C57BL/6N * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cep55tm1c(EUCOMM)Hmgu mutation (0 available); any Cep55 mutation (96 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• cell survival in adult intestine is normal





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
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last database update
01/19/2021
MGI 6.16
The Jackson Laboratory