All Phenotypes Tg(Vil1-cre)20Syr MGI Mouse

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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

51 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Epas1^tm1Yms/Epas1^tm1Yms Tg(Vil1-cre)20Syr/0	B6.Cg-Epas1^tm1Yms Tg(Vil1-cre)20Syr	MGI:5446038
cn2	H2az1^tm1.1Hko/H2az1^tm1.1Hko H2az2^tm1.1Hko/H2az2^tm1.1Hko Tg(Vil1-cre)20Syr/0	B6.Cg-H2az1^tm1.1Hko H2az2^tm1.1Hko Tg(Vil1-cre)20Syr	MGI:6360248
cn3	Hif1a^tm1Stom/Hif1a^tm1Stom Tg(Vil1-cre)20Syr/0	B6.Cg-Hif1a^tm1Stom Tg(Vil1-cre)20Syr	MGI:7310211
cn4	Abcb7^tm1Mdf/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	Abcb7^tm1Mdf/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
cn6	Cdh1^tm1.1Mpst/Cdh1^tm2Kem Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺ Tg(Vil1-cre)20Syr/0	involves: 129 * C57BL/6 * DBA/2	MGI:4822000
cn7	Cdh1^tm2Kem/Cdh1⁺ Smad4^tm2.1Cxd/Smad4^tm2.1Cxd Trp53^tm1Brn/Trp53^tm1Brn Tg(Vil1-cre)20Syr/0	involves: 129 * C57BL/6 * DBA/2	MGI:5634401
cn8	Bmi1^tm1.1Lees/Bmi1^tm1.1Lees Apc^tm2Cip/Apc⁺ Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2	MGI:5532577
cn9	Smad4^tm2.1Cxd/Smad4^tm2.1Cxd Trp53^tm1Brn/Trp53^tm1Brn Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2	MGI:5634402
cn10	Bmi1^tm1Brn/Bmi1^tm1Brn Apc^tm2Cip/Apc⁺ Cdkn2a^tm1Cjs/Cdkn2a^tm1Cjs Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * DBA/2	MGI:5532576
cn11	Mbd3^tm2Bh/Mbd3^tm2Bh Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * C57BL/6 * DBA/2	MGI:4887392
cn12	Nf2^tm2Gth/Nf2^tm2Gth Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * C57BL/6 * DBA/2	MGI:3850478
cn13	Apc^tm2.1Cip/Apc⁺ Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * C57BL/6 * DBA/2	MGI:4461183
cn14	Pikfyve^tm2.1Tssk/Pikfyve^tm2.1Tssk Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * C57BL/6 * DBA/2	MGI:5474983
cn15	Bmi1^tm1Brn/Bmi1^tm1Brn Apc^tm2Cip/Apc⁺ Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * C57BL/6 * DBA/2	MGI:5532574
cn16	Dsc2^tm1.1Leu/Dsc2^tm1.1Leu Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * C57BL/6 * DBA/2	MGI:6693361
cn17	Rprd1b^tm1Tshu/Rprd1b^tm1Tshu Lgr5^{tm1(cre/ERT2)Cle}/Lgr5⁺ Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * C57BL/6 * DBA/2	MGI:6822318
cn18	E2f4^tm2.1Lees/E2f4^tm2.1Lees E2f5^tm1Dli/E2f5⁺ Tg(Vil1-cre)20Syr/0	involves: 129S1/Sv * 129S4/SvJae * C57BL/6 * DBA/2	MGI:5706798
cn19	Lrp5^tm1Kry/Lrp5^tm1Kry Tph1^tm1Kry/Tph1⁺ Tg(Vil1-cre)20Syr/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2	MGI:3837415
cn20	Clcn3^tm1Tjj/Clcn3^tm1Tjj Clcn5^tm6.1Tjj/Y Tg(Vil1-cre)20Syr/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2	MGI:4834499
cn21	Neurog3^tm1Fgu/Neurog3^tm3.1Ggr Tg(Vil1-cre)20Syr/0	involves: 129S2/SvPas * C57BL/6 * CD-1 * DBA/2 * SJL	MGI:4460260
cn22	Neurog3^tm3.1Ggr/Neurog3^tm3.1Ggr Tg(Vil1-cre)20Syr/0	involves: 129S2/SvPas * C57BL/6 * CD-1 * DBA/2 * SJL	MGI:4460261
cn23	Htr1b^tm1Rhn/Htr1b⁺ Tph1^tm1Kry/Tph1⁺ Tg(Vil1-cre)20Syr/0	involves: 129S2/SvPas * C57BL/6 * DBA/2	MGI:3837413
cn24	Gt(ROSA)26Sor^{tm2(Rnf187)Jhai}/Gt(ROSA)26Sor⁺ Kras^tm4Tyj/Kras⁺ Tg(Vil1-cre)20Syr/0	involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2	MGI:5013409
cn25	Slc40a1^tm2Nca/Slc40a1^tm2Nca Tg(Vil1-cre)20Syr/0	involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2	MGI:3771552
cn26	Tfrc^tm3.1Nca/Tfrc^tm3.1Nca Tg(Vil1-cre)20Syr/0	involves: 129S4/SvJae * C57BL/6 * CD-1 * DBA/2	MGI:5689322
cn27	Gt(ROSA)26Sor^{tm1(Tfrc*)Nca}/Gt(ROSA)26Sor⁺ Tfrc^tm3.1Nca/Tfrc^tm3.1Nca Tg(Vil1-cre)20Syr/0	involves: 129S4/SvJae * C57BL/6 * CD-1 * DBA/2	MGI:5689324
cn28	E2f4^tm2.1Lees/E2f4^tm2.1Lees Tg(Vil1-cre)20Syr/0	involves: 129S4/SvJae * C57BL/6 * DBA/2	MGI:5706796
cn29	Slc11a2^tm2Nca/Slc11a2^tm2Nca Tg(Vil1-cre)20Syr/?	involves: 129S6.129S4-Slc11a2^tm2Nca * C57BL/6 * DBA/2	MGI:3578660
cn30	Apc^Min/Apc⁺ Gt(ROSA)26Sor^{tm2(Rnf187)Jhai}/Gt(ROSA)26Sor⁺ Tg(Vil1-cre)20Syr/0	involves: 129S6/SvEvTac * C57BL/6 * DBA/2	MGI:5013408
cn31	Dsg2^tm3.1Leu/Dsg2^tm3.1Leu Tg(Vil1-cre)20Syr/0	involves: 129S7/SvEvBrd * C57BL/6 * DBA/2	MGI:6693360
cn32	Msh2^tm1Rak/Msh2^tm2.1Rak Tg(Vil1-cre)20Syr/0	involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * DBA/2 * SJL	MGI:4460268
cn33	Clcn4^tm1Tjj/Clcn4^tm1Tjj Clcn5^tm6.1Tjj/Y Tg(Vil1-cre)20Syr/0	involves: 129/Sv * C57BL/6 * DBA/2	MGI:4834500
cn34	Msh2^tm2.1Rak/Msh2^tm3.1Rak Tg(Vil1-cre)20Syr/0	involves: 129/Sv * C57BL/6 * DBA/2 * SJL	MGI:4460267
cn35	Msh2^tm2.1Rak/Msh2^tm2.1Rak Tg(Vil1-cre)20Syr/0	involves: 129/Sv * C57BL/6 * FVB/N * SJL	MGI:4460266
cn36	Arnt^tm1.1Gonz/Arnt^tm1.1Gonz Tg(Vil1-cre)20Syr/0	involves: 129X1/SvJ * C57BL/6 * DBA/2	MGI:5446037
cn37	Cdhr2^{tm1c(EUCOMM)Hmgu}/Cdhr2^{tm1c(EUCOMM)Hmgu} Tg(Vil1-cre)20Syr/0	involves: C57BL/6 * C57BL/6N * DBA/2	MGI:6363536
cn38	St18^{tm1c(KOMP)Wtsi}/St18^{tm1c(KOMP)Wtsi} Tg(Vil1-cre)20Syr/0	involves: C57BL/6 * C57BL/6N * DBA/2	MGI:6489912
cn39	Btnl6^em1Ahay/Btnl6^em1Ahay Tg(Vil1-cre)20Syr/0	involves: C57BL/6 * DBA/2	MGI:7545310
cn40	Tg(Vil1-cre)20Syr/0 Vmp1^tm1.1Arte/Vmp1^tm1.1Arte	involves: C57BL/6 * DBA/2	MGI:6386823
cn41	Apc^tm1Tyj/Apc⁺ Tg(Vil1-cre)20Syr/0	involves: C57BL/6 * DBA/2	MGI:4461182
cn42	Lrp5^tm2Kry/Lrp5⁺ Tg(Vil1-cre)20Syr/0	involves: C57BL/6 * DBA/2	MGI:3837404
cn43	Lrp5^{tm3(Lrp5)Kry}/Lrp5^{tm3(Lrp5)Kry} Tg(Vil1-cre)20Syr/0	involves: C57BL/6 * DBA/2	MGI:3837405
cn44	Znhit1^tm1.1Nju/Znhit1^tm1.1Nju Tg(Vil1-cre)20Syr/0	involves: C57BL/6 * DBA/2	MGI:6360245
cn45	Nras^tm1Tyj/Nras⁺ Tg(Vil1-cre)20Syr/0	involves: C57BL/6 * DBA/2	MGI:3776027
cn46	Rprd1b^tm1Tshu/Rprd1b^tm1Tshu Tg(Vil1-cre)20Syr/0	involves: C57BL/6 * DBA/2	MGI:6822317
cn47	Tph1^tm1Kry/Tph1^tm1Kry Tg(Vil1-cre)20Syr/0	involves: C57BL/6 * DBA/2	MGI:3837407
cn48	Lrp5^tm2Kry/Lrp5^tm2Kry Tg(Vil1-cre)20Syr/0	involves: C57BL/6 * DBA/2	MGI:3837403
cn49	Gt(ROSA)26Sor^{tm2(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
cn50	Gt(ROSA)26Sor^{tm2(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
cn51	Cep55^{tm1c(EUCOMM)Hmgu}/Cep55^{tm1c(EUCOMM)Hmgu} Tg(Vil1-cre)20Syr/0	involves: C57BL/6N * DBA/2	MGI:6458516

Allelic Composition	Epas1^tm1Yms/Epas1^tm1Yms Tg(Vil1-cre)20Syr/0
Genetic Background	B6.Cg-Epas1^tm1Yms Tg(Vil1-cre)20Syr

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Epas1^tm1Yms mutation (0 available); any Epas1 mutation (66 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

hematopoietic system

decreased erythrocyte cell number ( J:189504 )

decreased hematocrit ( J:189504 )

decreased hemoglobin content ( J:189504 )

homeostasis/metabolism

decreased circulating iron level ( J:189504 )

Allelic Composition	H2az1^tm1.1Hko/H2az1^tm1.1Hko H2az2^tm1.1Hko/H2az2^tm1.1Hko Tg(Vil1-cre)20Syr/0
Genetic Background	B6.Cg-H2az1^tm1.1Hko H2az2^tm1.1Hko Tg(Vil1-cre)20Syr

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2az1^tm1.1Hko mutation (0 available); any H2az1 mutation (13 available)
H2az2^tm1.1Hko mutation (0 available); any H2az2 mutation (26 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

decreased body weight ( J:276456 )

digestive/alimentary system

abnormal crypts of Lieberkuhn morphology ( J:276456 )

• crypt cells fail to form intestinal organoids in vitro

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:276456 )

• crypt cells fail to form intestinal organoids in vitro

Allelic Composition	Hif1a^tm1Stom/Hif1a^tm1Stom Tg(Vil1-cre)20Syr/0
Genetic Background	B6.Cg-Hif1a^tm1Stom Tg(Vil1-cre)20Syr

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm1Stom mutation (0 available); any Hif1a mutation (50 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

decreased susceptibility to induced hypothermia ( J:325395 )

• higher rectal temperature after cold challenge in mice fed a high-fat diet following a more significant drop in inguinal region

• however, response to is restored following oral or rectal administration of lactate

decreased circulating insulin level ( J:325395 )

• in fasted mice fed a high-fat diet

increased energy expenditure ( J:325395 )

• after cold challenge in mice fed a high-fat diet

• however, treatment with lactate restores normal energy expenditure

decreased susceptibility to diet-induced obesity ( J:325395 )

• despite equivalent food intake, mice fed a high-fat diet exhibit improved body weight gain and body fat content compared with control mice

increased oxygen consumption ( J:325395 )

• in the inguinal fat and epididymal fat of mice fed a high-fat diet after cold challenge along with increased mitochondrial CK activity

• however, treatment with lactate restores normal adaptive thermogenesis

increased respiratory quotient ( J:325395 )

• after cold challenge in mice fed a high-fat diet

• however, treatment with lactate restores normal RER

improved glucose tolerance ( J:325395 )

• in mice fed a high-fat diet

increased insulin sensitivity ( J:325395 )

• in mice fed a high-fat diet

increased bile salt level ( J:325395 )

• especially conjugated bile acids TCA and tauro-beta-muricholic acid, and precursor DCA in mice fed a high-fat diet compared with control mice

digestive/alimentary system

abnormal gut flora balance ( J:325395 )

• mice fed a high-fat diet exhibit inhibition of B. vulgatus and enrichment of R. torques associated with reduction in intestinal lactate levels compared with control mice

adipose tissue

decreased body fat mass ( J:325395 )

• in mice fed a high-fat diet

growth/size/body

decreased body fat mass ( J:325395 )

• in mice fed a high-fat diet

decreased susceptibility to diet-induced obesity ( J:325395 )

• despite equivalent food intake, mice fed a high-fat diet exhibit improved body weight gain and body fat content compared with control mice

Allelic Composition	Abcb7^tm1Mdf/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:
Abcb7^tm1Mdf mutation (1 available); any Abcb7 mutation (13 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

prenatal lethality, complete penetrance ( J:106838 )

Allelic Composition	Abcb7^tm1Mdf/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:
Abcb7^tm1Mdf mutation (1 available); any Abcb7 mutation (13 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

prenatal lethality, complete penetrance ( J:106838 )

Allelic Composition	Cdh1^tm1.1Mpst/Cdh1^tm2Kem Gt(ROSA)26Sor^tm1Sor/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:
Cdh1^tm1.1Mpst mutation (0 available); any Cdh1 mutation (173 available)
Cdh1^tm2Kem mutation (1 available); any Cdh1 mutation (173 available)
Gt(ROSA)26Sor^tm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

normal phenotype

no abnormal phenotype detected ( J:163273 )

Allelic Composition	Cdh1^tm2Kem/Cdh1⁺ Smad4^tm2.1Cxd/Smad4^tm2.1Cxd Trp53^tm1Brn/Trp53^tm1Brn 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:
Cdh1^tm2Kem mutation (1 available); any Cdh1 mutation (173 available)
Smad4^tm2.1Cxd mutation (2 available); any Smad4 mutation (48 available)
Tg(Vil1-cre)20Syr mutation (4 available)
Trp53^tm1Brn mutation (18 available); any Trp53 mutation (240 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased intestinal adenocarcinoma incidence ( J:212549 )

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

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:212549 )

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

Allelic Composition	Bmi1^tm1.1Lees/Bmi1^tm1.1Lees Apc^tm2Cip/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:
Apc^tm2Cip mutation (0 available); any Apc mutation (158 available)
Bmi1^tm1.1Lees mutation (1 available); any Bmi1 mutation (31 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

decreased alimentary system tumor incidence ( J:204354 )

• reduced visible and total lesions in the small intestine

decreased colon tumor incidence ( J:204354 )

decreased intestinal adenoma incidence ( J:204354 )

digestive/alimentary system

decreased alimentary system tumor incidence ( J:204354 )

• reduced visible and total lesions in the small intestine

decreased colon tumor incidence ( J:204354 )

decreased intestinal adenoma incidence ( J:204354 )

cellular

cellular phenotype ( J:204354 )

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

Allelic Composition	Smad4^tm2.1Cxd/Smad4^tm2.1Cxd Trp53^tm1Brn/Trp53^tm1Brn 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:
Smad4^tm2.1Cxd mutation (2 available); any Smad4 mutation (48 available)
Tg(Vil1-cre)20Syr mutation (4 available)
Trp53^tm1Brn mutation (18 available); any Trp53 mutation (240 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased intestinal adenocarcinoma incidence ( J:212549 )

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

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:212549 )

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

Allelic Composition	Bmi1^tm1Brn/Bmi1^tm1Brn Apc^tm2Cip/Apc⁺ Cdkn2a^tm1Cjs/Cdkn2a^tm1Cjs 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:
Apc^tm2Cip mutation (0 available); any Apc mutation (158 available)
Bmi1^tm1Brn mutation (2 available); any Bmi1 mutation (31 available)
Cdkn2a^tm1Cjs mutation (7 available); any Cdkn2a mutation (67 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

cachexia ( J:204354 )

• found in some animals by 90 days of age

behavior/neurological

hunched posture ( J:204354 )

• hunching appears in some animals at 90 days of age

neoplasm

increased intestinal adenoma incidence ( J:204354 )

• increased size and number of small intestine adenomas

digestive/alimentary system

increased intestinal adenoma incidence ( J:204354 )

• increased size and number of small intestine adenomas

Allelic Composition	Mbd3^tm2Bh/Mbd3^tm2Bh 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:
Mbd3^tm2Bh mutation (2 available); any Mbd3 mutation (58 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

digestive/alimentary system

abnormal small intestinal crypt cell proliferation ( J:167984 )

• increase in intestinal progenitor cell proliferation in the crypts

increased susceptibility to induced colitis ( J:167984 )

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

neoplasm

increased incidence of tumors by chemical induction ( J:167984 )

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

increased tumor growth/size ( J:167984 )

• tumors induced by azoxymethane and DSS treatment are increased in size compared to controls

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:167984 )

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

immune system

increased susceptibility to induced colitis ( J:167984 )

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

cellular

abnormal small intestinal crypt cell proliferation ( J:167984 )

• increase in intestinal progenitor cell proliferation in the crypts

Allelic Composition	Nf2^tm2Gth/Nf2^tm2Gth 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:
Nf2^tm2Gth mutation (3 available); any Nf2 mutation (65 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:150071 )

• mice die by 10 months of age

lethality throughout fetal growth and development, incomplete penetrance ( J:150071 )

• mice occasionally die between E17 and P3

perinatal lethality, incomplete penetrance ( J:150071 )

• mice occasionally die between E17 and P3

postnatal lethality, incomplete penetrance ( J:150071 )

• mice occasionally die between E17 and P3

• fewer than expected mice survive until weaning

neoplasm

increased renal carcinoma incidence ( J:150071 )

• 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 Nf2^tm2Gth homozygotes

• however, treatment with erlotinib reduces cell proliferation

growth/size/body

decreased body size ( J:150071 )

renal/urinary system

increased renal carcinoma incidence ( J:150071 )

• 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 Nf2^tm2Gth homozygotes

• however, treatment with erlotinib reduces cell proliferation

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

Allelic Composition	Apc^tm2.1Cip/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:
Apc^tm2.1Cip mutation (2 available); any Apc mutation (158 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased intestinal adenoma incidence ( J:160399 )

increased colon adenoma incidence ( J:160399 )

digestive/alimentary system

increased intestinal adenoma incidence ( J:160399 )

increased colon adenoma incidence ( J:160399 )

Allelic Composition	Pikfyve^tm2.1Tssk/Pikfyve^tm2.1Tssk 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:
Pikfyve^tm2.1Tssk mutation (0 available); any Pikfyve mutation (116 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

lethality, incomplete penetrance ( J:193689 )

• only 20% of mice born alive survive beyond 100 days

premature death ( J:193689 )

• only 20% of mice born alive survive beyond 100 days

prenatal lethality, incomplete penetrance ( J:193689 )

• recovered at a lower than expected Mendelian frequency

digestive/alimentary system

diarrhea ( J:193689 )

melena ( J:193689 )

abnormal enterocyte morphology ( J:193689 )

• 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

abnormal small intestinal microvillus morphology ( J:193689 )

• sparse in number

decreased small intestinal microvillus size ( J:193689 )

• short

intestinal fibrosis ( J:193689 )

• overt fibrosis of the muscularis mucosa

intestinal inflammation ( J:193689 )

• lymphocyte infiltration is prominent in both the mucosa and submucosa

homeostasis/metabolism

decreased circulating free fatty acids level ( J:193689 )

abnormal circulating enzyme level ( J:193689 )

• decrease in circulating choline esterase levels

decreased circulating serum albumin level ( J:193689 )

decreased circulating total protein level ( J:193689 )

growth/size/body

decreased body weight ( J:193689 )

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

behavior/neurological

lethargy ( J:193689 )

hunched posture ( J:193689 )

integument

disheveled coat ( J:193689 )

immune system

intestinal inflammation ( J:193689 )

• 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

Allelic Composition	Bmi1^tm1Brn/Bmi1^tm1Brn Apc^tm2Cip/Apc⁺ Tg(Vil1-cre)20Syr/0
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * DBA/2

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

decreased alimentary system tumor incidence ( J:204354 )

• 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

decreased colon tumor incidence ( J:204354 )

• also reduced at 120 days

decreased intestinal adenoma incidence ( J:204354 )

• 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 ( J:204354 )

• increased apoptosis in smaller adenomas but not larger ones at 90 days

• apoptosis is also increased in non tumor tissue

digestive/alimentary system

decreased alimentary system tumor incidence ( J:204354 )

• 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

decreased colon tumor incidence ( J:204354 )

• also reduced at 120 days

decreased intestinal adenoma incidence ( J:204354 )

• 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

Allelic Composition	Dsc2^tm1.1Leu/Dsc2^tm1.1Leu 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:
Dsc2^tm1.1Leu mutation (0 available); any Dsc2 mutation (80 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

digestive/alimentary system

digestive/alimentary phenotype ( J:302333 )

N	• normal intestinal histology • normal desmosomal plaques in intestines • normal intestinal permeability • normal susceptibility to dextran sodium sulfate (DSS)-induced colitis

growth/size/body

growth/size/body region phenotype ( J:302333 )

N	• no gross abnormalities

immune system

immune system phenotype ( J:302333 )

N	• normal susceptibility to dextran sodium sulfate (DSS)-induced colitis

Allelic Composition	Rprd1b^tm1Tshu/Rprd1b^tm1Tshu Lgr5^{tm1(cre/ERT2)Cle}/Lgr5⁺ 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:
Lgr5^{tm1(cre/ERT2)Cle} mutation (1 available); any Lgr5 mutation (58 available)
Rprd1b^tm1Tshu mutation (0 available); any Rprd1b mutation (16 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

digestive/alimentary system

abnormal digestive system development ( J:300857 )

• decreased Lgr5-GFP+ cells pre and post tamoxifen treatment

• tamoxifen-treated cultured intestinal crypt organoids exhibit fewer outgrowths and fail to reform after disaggregation unlike control cultures

Allelic Composition	E2f4^tm2.1Lees/E2f4^tm2.1Lees E2f5^tm1Dli/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:
E2f4^tm2.1Lees mutation (1 available); any E2f4 mutation (21 available)
E2f5^tm1Dli mutation (1 available); any E2f5 mutation (13 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

reproductive system

reproductive system phenotype ( J:228346 )

N	• male mice exhibit normal spermatogenesis

dilated rete testis ( J:228346 )

• often contains many spermatozoa

abnormal seminiferous tubule epithelium morphology ( J:228346 )

• atrophic

dilated seminiferous tubule ( J:228346 )

• with dilation at that the expense of the epithelium

abnormal efferent ductules of testis morphology ( J:228346 )

• 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

abnormal epididymis morphology ( J:228346 )

• no spermatozoa are detected in the epididymis

male infertility ( J:228346 )

endocrine/exocrine glands

dilated rete testis ( J:228346 )

• often contains many spermatozoa

abnormal seminiferous tubule epithelium morphology ( J:228346 )

• atrophic

dilated seminiferous tubule ( J:228346 )

• with dilation at that the expense of the epithelium

Allelic Composition	Lrp5^tm1Kry/Lrp5^tm1Kry Tph1^tm1Kry/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:
Lrp5^tm1Kry mutation (0 available); any Lrp5 mutation (82 available)
Tg(Vil1-cre)20Syr mutation (4 available)
Tph1^tm1Kry mutation (0 available); any Tph1 mutation (41 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

skeleton

skeleton phenotype ( J:146078 )

N	• loss of expression of 1 copy of Tph1 in the gut rescues the bone phenotype seen in Lrp5 null mice

Allelic Composition	Clcn3^tm1Tjj/Clcn3^tm1Tjj Clcn5^tm6.1Tjj/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:
Clcn3^tm1Tjj mutation (0 available); any Clcn3 mutation (120 available)
Clcn5^tm6.1Tjj mutation (0 available); any Clcn5 mutation (17 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

renal/urinary system

abnormal renal protein reabsorption ( J:164474 )

• mice exhibit reduced endocytic uptake of beta-lactoglobulin by proximal tubule cells similar to in Clcn5^tm1Tjj homozygotes

homeostasis/metabolism

abnormal renal protein reabsorption ( J:164474 )

• mice exhibit reduced endocytic uptake of beta-lactoglobulin by proximal tubule cells similar to in Clcn5^tm1Tjj homozygotes

Allelic Composition	Neurog3^tm1Fgu/Neurog3^tm3.1Ggr 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:
Neurog3^tm1Fgu mutation (0 available); any Neurog3 mutation (19 available)
Neurog3^tm3.1Ggr mutation (0 available); any Neurog3 mutation (19 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Loss of enteroendocrine cells in Neurog3^tm1Fgu/Neurog3^tm3.1Ggr Tg(Vil1-cre)20Syr/0 and Neurog3^tm3.1Ggr/Neurog3^tm3.1Ggr Tg(Vil1-cre)20Syr/0 mice

mortality/aging

postnatal lethality, incomplete penetrance ( J:161480 )

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

digestive/alimentary system

abnormal intestinal goblet cell morphology ( J:161480 )

• 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

abnormal small intestinal crypt cell proliferation ( J:161480 )

• 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

abnormal intestine development ( J:161480 )

• 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

abnormal intestinal enteroendocrine cell morphology ( J:161480 )

• as early as embryogenesis, mice lack enteroendocrine progenitors along the proximal-distal axis of the intestine unlike in wild-type mice

steatorrhea ( J:161480 )

• mice excrete yellowish stool unlike wild-type mice

diarrhea ( J:161480 )

• surviving mice exhibit soft stool that does not cease with age unlike in wild-type mice

abnormal small intestine crypts of Lieberkuhn morphology ( J:161480 )

• small intestine crypts are disorganized, larger, and more abundant than in wild-type mice

abnormal large intestine morphology ( J:161480 )

• the large intestine exhibits a reduction in the length of glands of up to 1.5 times compared with wild-type mice

abnormal small intestinal villus morphology ( J:161480 )

• villi are blunted or club shaped with frequent dilation and strong detachment of the epithelium from the basement membrane unlike in wild-type mice

abnormal small intestinal microvillus morphology ( J:161480 )

• 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

decreased small intestinal microvillus size ( J:161480 )

• 60% shorter than in wild-type mice

increased defecation amount ( J:161480 )

• mice produce more feces compared with wild-type mice

abnormal intestinal lipid absorption ( J:161480 )

• impaired

abnormal intestinal transit time ( J:161480 )

• intestinal transit time is increased 2.3-fold compared to in wild-type mice

homeostasis/metabolism

steatorrhea ( J:161480 )

• mice excrete yellowish stool unlike wild-type mice

abnormal intestinal lipid absorption ( J:161480 )

• impaired

increased blood urea nitrogen level ( J:161480 )

• slightly

increased circulating bicarbonate level ( J:161480 )

• slightly

decreased circulating glucose level ( J:161480 )

• 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

decreased circulating cholesterol level ( J:161480 )

decreased circulating HDL cholesterol level ( J:161480 )

decreased circulating triglyceride level ( J:161480 )

decreased circulating serum albumin level ( J:161480 )

improved glucose tolerance ( J:161480 )

• 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

increased insulin sensitivity ( J:161480 )

• slightly at 14 and 17 weeks

• insulin-mediated hypoglycemic response is blunted compared to in wild-type mice

growth/size/body

decreased birth weight ( J:161480 )

decreased body mass index ( J:161480 )

increased lean body mass ( J:161480 )

decreased body size ( J:161480 )

postnatal growth retardation ( J:161480 )

adipose tissue

decreased total body fat amount ( J:161480 )

abnormal abdominal fat pad morphology ( J:161480 )

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

endocrine/exocrine glands

abnormal small intestine crypts of Lieberkuhn morphology ( J:161480 )

• small intestine crypts are disorganized, larger, and more abundant than in wild-type mice

abnormal pancreatic islet morphology ( J:161480 )

• mice exhibit more medium and large islets with centrally located alpha cells than in wild-type mice

small pancreatic islets ( J:161480 )

• mice exhibit a shift from large to single islets compared with wild-type mice

cellular

abnormal intestinal goblet cell morphology ( J:161480 )

• 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

abnormal small intestinal crypt cell proliferation ( J:161480 )

• 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

Allelic Composition	Neurog3^tm3.1Ggr/Neurog3^tm3.1Ggr 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:
Neurog3^tm3.1Ggr mutation (0 available); any Neurog3 mutation (19 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Loss of enteroendocrine cells in Neurog3^tm1Fgu/Neurog3^tm3.1Ggr Tg(Vil1-cre)20Syr/0 and Neurog3^tm3.1Ggr/Neurog3^tm3.1Ggr Tg(Vil1-cre)20Syr/0 mice

mortality/aging

postnatal lethality, incomplete penetrance ( J:161480 )

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

homeostasis/metabolism

steatorrhea ( J:161480 )

• mice excrete yellowish stool unlike wild-type mice

abnormal intestinal lipid absorption ( J:161480 )

• impaired

increased blood urea nitrogen level ( J:161480 )

• slightly

increased circulating bicarbonate level ( J:161480 )

• slightly

decreased circulating glucose level ( J:161480 )

• 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

decreased circulating cholesterol level ( J:161480 )

decreased circulating HDL cholesterol level ( J:161480 )

decreased circulating triglyceride level ( J:161480 )

decreased circulating serum albumin level ( J:161480 )

improved glucose tolerance ( J:161480 )

• 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

increased insulin sensitivity ( J:161480 )

• slightly at 14 and 17 weeks

• insulin-mediated hypoglycemic response is blunted compared to in wild-type mice

digestive/alimentary system

abnormal intestinal goblet cell morphology ( J:161480 )

• 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

abnormal small intestinal crypt cell proliferation ( J:161480 )

• 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

abnormal intestine development ( J:161480 )

• 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

abnormal intestinal enteroendocrine cell morphology ( J:161480 )

• as early as embryogenesis, mice lack enteroendocrine progenitors along the proximal-distal axis of the intestine unlike in wild-type mice

steatorrhea ( J:161480 )

• mice excrete yellowish stool unlike wild-type mice

diarrhea ( J:161480 )

• surviving mice exhibit soft stool that does not cease with age unlike in wild-type mice

abnormal small intestine crypts of Lieberkuhn morphology ( J:161480 )

• small intestine crypts are disorganized, larger, and more abundant than in wild-type mice

abnormal large intestine morphology ( J:161480 )

• the large intestine exhibits a reduction in the length of glands of up to 1.5 times compared with wild-type mice

abnormal small intestinal villus morphology ( J:161480 )

• villi are blunted or club shaped with frequent dilation and strong detachment of the epithelium from the basement membrane unlike in wild-type mice

abnormal small intestinal microvillus morphology ( J:161480 )

• 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

decreased small intestinal microvillus size ( J:161480 )

• 60% shorter than in wild-type mice

increased defecation amount ( J:161480 )

• mice produce more feces compared with wild-type mice

abnormal intestinal lipid absorption ( J:161480 )

• impaired

abnormal intestinal transit time ( J:161480 )

• intestinal transit time is increased 2.3-fold compared to in wild-type mice

growth/size/body

decreased birth weight ( J:161480 )

decreased body mass index ( J:161480 )

increased lean body mass ( J:161480 )

decreased body size ( J:161480 )

postnatal growth retardation ( J:161480 )

adipose tissue

decreased total body fat amount ( J:161480 )

abnormal abdominal fat pad morphology ( J:161480 )

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

endocrine/exocrine glands

abnormal small intestine crypts of Lieberkuhn morphology ( J:161480 )

• small intestine crypts are disorganized, larger, and more abundant than in wild-type mice

abnormal pancreatic islet morphology ( J:161480 )

• mice exhibit more medium and large islets with centrally located alpha cells than in wild-type mice

small pancreatic islets ( J:161480 )

• mice exhibit a shift from large to single islets compared with wild-type mice

cellular

abnormal intestinal goblet cell morphology ( J:161480 )

• 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

abnormal small intestinal crypt cell proliferation ( J:161480 )

• 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

Allelic Composition	Htr1b^tm1Rhn/Htr1b⁺ Tph1^tm1Kry/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:
Htr1b^tm1Rhn mutation (3 available); any Htr1b mutation (26 available)
Tg(Vil1-cre)20Syr mutation (4 available)
Tph1^tm1Kry mutation (0 available); any Tph1 mutation (41 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

skeleton

increased bone mass ( J:146078 )

• phenotype is the same as in mice homozygous null for Htr1b and mice conditional null for Tph1 in the gut

Allelic Composition	Gt(ROSA)26Sor^{tm2(Rnf187)Jhai}/Gt(ROSA)26Sor⁺ Kras^tm4Tyj/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)26Sor^{tm2(Rnf187)Jhai} mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Kras^tm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

digestive/alimentary system

abnormal enterocyte proliferation ( J:173145 )

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

cellular

abnormal enterocyte proliferation ( J:173145 )

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

Allelic Composition	Slc40a1^tm2Nca/Slc40a1^tm2Nca 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:
Slc40a1^tm2Nca mutation (1 available); any Slc40a1 mutation (54 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

prenatal lethality, complete penetrance ( J:129846 )

• no mice are found at birth due to recombination in the extraembryonic visceral endoderm

Allelic Composition	Tfrc^tm3.1Nca/Tfrc^tm3.1Nca 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:
Tfrc^tm3.1Nca mutation (2 available); any Tfrc mutation (64 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

postnatal lethality, complete penetrance ( J:224823 )

• mice die before P3 with variable timing

• treatment with iron dextran does not extend lifespan

digestive/alimentary system

abnormal enterocyte proliferation ( J:224823 )

• reduced proliferation in intervillous regions

melena ( J:224823 )

abnormal intestine morphology ( J:224823 )

• mice exhibit milk in intestinal lumen, shorter intestines with apparent melena compared with wild-type mice

abnormal enterocyte morphology ( J:224823 )

• larger intestinal epithelial cells contain vacuole-like lipid accumulation than in wild-type cells

abnormal colon morphology ( J:224823 )

• 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

decreased colon length ( J:224823 )

• reduced length with apparent melena

abnormal small intestine morphology ( J:224823 )

abnormal duodenum morphology ( J:224823 )

blunted small intestinal villi ( J:224823 )

• blunted villi

distended stomach ( J:224823 )

• with milk

growth/size/body

decreased body size ( J:224823 )

• mice fail to thrice and are runted by P1

cellular

abnormal enterocyte proliferation ( J:224823 )

• reduced proliferation in intervillous regions

Allelic Composition	Gt(ROSA)26Sor^{tm1(Tfrc*)Nca}/Gt(ROSA)26Sor⁺ Tfrc^tm3.1Nca/Tfrc^tm3.1Nca 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)26Sor^{tm1(Tfrc*)Nca} mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Tfrc^tm3.1Nca mutation (2 available); any Tfrc mutation (64 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

postnatal lethality, incomplete penetrance ( J:224823 )

• some mice die postnatally

• however, most mice are alive at 2 months

digestive/alimentary system

abnormal digestive system morphology ( J:224823 )

• mice that die exhibit the same phenotype as Tfrc^tm3.1Nca/Tfrc^tm3.1Nca Tg(Vil-cre)20Syr mice

• however, mice that survive at 2 months exhibit normal architecture and proliferation of crypt intestinal epithelial cells

Allelic Composition	E2f4^tm2.1Lees/E2f4^tm2.1Lees 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:
E2f4^tm2.1Lees mutation (1 available); any E2f4 mutation (21 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

normal phenotype

no abnormal phenotype detected ( J:228346 )

• mice are viable and fertile with normal intestinal morphology and efferent duct epithelium

Allelic Composition	Slc11a2^tm2Nca/Slc11a2^tm2Nca Tg(Vil1-cre)20Syr/?
Genetic Background	involves: 129S6.129S4-Slc11a2^tm2Nca * C57BL/6 * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc11a2^tm2Nca mutation (1 available); any Slc11a2 mutation (38 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

hematopoietic system

extramedullary hematopoiesis ( J:98088 )

• sinusoid areas of the liver particularly

• dysplastic erythropoiesis in the spleen

anemia ( J:98088 )

• progressive anemia developed after birth

• profound but not as severe as in knock-out mice

abnormal erythrocyte morphology ( J:98088 )

abnormal spleen morphology ( J:98088 )

enlarged spleen ( J:98088 )

decreased spleen iron level ( J:98088 )

• decreased non-heme iron in the spleen

increased spleen red pulp amount ( J:98088 )

• expanded red pulp

homeostasis/metabolism

decreased heart iron level ( J:98088 )

• decreased non-heme iron in the heart

decreased spleen iron level ( J:98088 )

• decreased non-heme iron in the spleen

decreased brain iron level ( J:98088 )

• diminished non-heme iron levels in the brain

decreased kidney iron level ( J:98088 )

• decreased non-heme iron

decreased liver iron level ( J:98088 )

• decreased non-heme iron in the liver

cardiovascular system

decreased heart iron level ( J:98088 )

• decreased non-heme iron in the heart

enlarged heart ( J:98088 )

immune system

abnormal spleen morphology ( J:98088 )

enlarged spleen ( J:98088 )

decreased spleen iron level ( J:98088 )

• decreased non-heme iron in the spleen

increased spleen red pulp amount ( J:98088 )

• expanded red pulp

liver/biliary system

decreased liver iron level ( J:98088 )

• decreased non-heme iron in the liver

renal/urinary system

decreased kidney iron level ( J:98088 )

• decreased non-heme iron

nervous system

decreased brain iron level ( J:98088 )

• diminished non-heme iron levels in the brain

growth/size/body

enlarged heart ( J:98088 )

enlarged spleen ( J:98088 )

Allelic Composition	Apc^Min/Apc⁺ Gt(ROSA)26Sor^{tm2(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:
Apc^Min mutation (12 available); any Apc mutation (158 available)
Gt(ROSA)26Sor^{tm2(Rnf187)Jhai} mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased gastrointestinal tumor incidence ( J:173145 )

• intestinal tumors are increased in number compared to in Apc^Min/Apc⁺ Tg(Vil-cre)20Syr

increased tumor growth/size ( J:173145 )

• intestinal tumors exhibit increased cell proliferation and size compared to in Apc^Min/Apc⁺ Tg(Vil-cre)20Syr

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:173145 )

• intestinal tumors are increased in number compared to in Apc^Min/Apc⁺ Tg(Vil-cre)20Syr

Allelic Composition	Dsg2^tm3.1Leu/Dsg2^tm3.1Leu Tg(Vil1-cre)20Syr/0
Genetic Background	involves: 129S7/SvEvBrd * C57BL/6 * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dsg2^tm3.1Leu mutation (0 available); any Dsg2 mutation (80 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

digestive/alimentary system

digestive/alimentary phenotype ( J:302333 )

N	• normal colon length and intestinal histology • no diarrhea • normal intestinal basal cell proliferation • no intestinal inflammation • normal desmosomal plaques in intestines

abnormal intestinal epithelium morphology ( J:302333 )

• wider intercellular spaces between desmosomal plaques in small and large intestine

• normal desmosomal plaques in intestines

increased susceptibility to induced colitis ( J:302333 )

• stronger inflammatory reaction, hyperproliferation and increased epithelial detachment and crypt elongation in intestines and higher fecal bacterial colony forming unit (CFU) count after Citrobacter rodentium exposure

• normal infection clearance after Citrobacter rodentium exposure

increased susceptibility to colitis induced morbidity/mortality ( J:302333 )

• shorter colon, more profound weight loss, intestinal lesions and bloody diarrhea after administration of low doses of dextran sodium sulfate (DSS)

• epithelial loss, edema, inflammatory reactions and goblet cell loss in intestines after administration of low doses of dextran sodium sulfate (DSS)

immune system

increased susceptibility to induced colitis ( J:302333 )

• normal infection clearance after Citrobacter rodentium exposure

increased susceptibility to colitis induced morbidity/mortality ( J:302333 )

• shorter colon, more profound weight loss, intestinal lesions and bloody diarrhea after administration of low doses of dextran sodium sulfate (DSS)

• epithelial loss, edema, inflammatory reactions and goblet cell loss in intestines after administration of low doses of dextran sodium sulfate (DSS)

growth/size/body

growth/size/body region phenotype ( J:302333 )

N	• normal postnatal weight gain and colon length

mortality/aging

increased susceptibility to colitis induced morbidity/mortality ( J:302333 )

• shorter colon, more profound weight loss, intestinal lesions and bloody diarrhea after administration of low doses of dextran sodium sulfate (DSS)

• epithelial loss, edema, inflammatory reactions and goblet cell loss in intestines after administration of low doses of dextran sodium sulfate (DSS)

Allelic Composition	Msh2^tm1Rak/Msh2^tm2.1Rak 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:
Msh2^tm1Rak mutation (1 available); any Msh2 mutation (95 available)
Msh2^tm2.1Rak mutation (1 available); any Msh2 mutation (95 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased gastrointestinal tumor incidence ( J:161577 )

• beginning at 6 months, mice develop intestinal tumors

• by 10 months, 50% of mice develop intestinal tumors

increased intestinal adenocarcinoma incidence ( J:161577 )

• 82% of tumors

increased intestinal adenoma incidence ( J:161577 )

• 18% of tumors

abnormal tumor morphology ( J:161577 )

• mice develop fewer and larger tumors than in Msh2^tm2.1Rak/Msh2^tm3.1Wed Tg(Vil-cre)20Syr mice

• tumors do not respond to treatment with cisplatin or FOLFOX unlike tumors from Msh2^tm2.1Rak/Msh2^tm3.1Wed Tg(Vil-cre)20Syr mice

homeostasis/metabolism

abnormal mismatch repair ( J:161577 )

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

abnormal physiological response to xenobiotic ( J:161577 )

• tumors do not respond to treatment with cisplatin or FOLFOX unlike tumors from Msh2^tm2.1Rak/Msh2^tm3.1Wed Tg(Vil-cre)20Syr mice

• FOLFOX-treated intestinal mucosa exhibit decreased apoptosis compared with similarly treated cells from Msh2^tm2.1Wed homozygotes and Msh2^tm2.1Rak/Msh2^tm3.1Wed Tg(Vil-cre)20Syr mice

cellular

abnormal mismatch repair ( J:161577 )

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

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:161577 )

• beginning at 6 months, mice develop intestinal tumors

• by 10 months, 50% of mice develop intestinal tumors

increased intestinal adenocarcinoma incidence ( J:161577 )

• 82% of tumors

increased intestinal adenoma incidence ( J:161577 )

• 18% of tumors

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

Allelic Composition	Clcn4^tm1Tjj/Clcn4^tm1Tjj Clcn5^tm6.1Tjj/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:
Clcn4^tm1Tjj mutation (0 available); any Clcn4 mutation (53 available)
Clcn5^tm6.1Tjj mutation (0 available); any Clcn5 mutation (17 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

renal/urinary system

abnormal renal protein reabsorption ( J:164474 )

• mice exhibit reduced endocytic uptake of beta-lactoglobulin by proximal tubule cells similar to in Clcn5^tm1Tjj homozygotes

homeostasis/metabolism

abnormal renal protein reabsorption ( J:164474 )

• mice exhibit reduced endocytic uptake of beta-lactoglobulin by proximal tubule cells similar to in Clcn5^tm1Tjj homozygotes

Allelic Composition	Msh2^tm2.1Rak/Msh2^tm3.1Rak 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:
Msh2^tm2.1Rak mutation (1 available); any Msh2 mutation (95 available)
Msh2^tm3.1Rak mutation (0 available); any Msh2 mutation (95 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased gastrointestinal tumor incidence ( J:161577 )

• beginning at 10 months, mice develop intestinal tumors

• by 13 months, 50% of mice develop intestinal tumors

increased intestinal adenocarcinoma incidence ( J:161577 )

• 63% of tumors

increased intestinal adenoma incidence ( J:161577 )

• 37% of tumors

abnormal tumor morphology ( J:161577 )

• mice develop more and smaller tumors than in Msh2^tm1Rak/Msh2^tm2.1Wed Tg(Vil-cre)20Syr mice

• tumors respond to treatment with cisplatin or FOLFOX unlike tumors from Msh2^tm1Rak/Msh2^tm2.1Wed Tg(Vil-cre)20Syr mice

homeostasis/metabolism

abnormal mismatch repair ( J:161577 )

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

abnormal physiological response to xenobiotic ( J:161577 )

• tumors respond to treatment with cisplatin or FOLFOX unlike tumors from Msh2^tm1Rak/Msh2^tm2.1Wed Tg(Vil-cre)20Syr mice

• FOLFOX-treated intestinal mucosa cells exhibit decreased apoptosis compared with similarly treated cells from Msh2^tm2.1Wed homozygotes but increased compared with similarly treated cell from Msh2^tm1Rak/Msh2^tm2.1Wed Tg(Vil-cre)20Syr mice

cellular

abnormal mismatch repair ( J:161577 )

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

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:161577 )

• beginning at 10 months, mice develop intestinal tumors

• by 13 months, 50% of mice develop intestinal tumors

increased intestinal adenocarcinoma incidence ( J:161577 )

• 63% of tumors

increased intestinal adenoma incidence ( J:161577 )

• 37% of tumors

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

Allelic Composition	Msh2^tm2.1Rak/Msh2^tm2.1Rak 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:
Msh2^tm2.1Rak mutation (1 available); any Msh2 mutation (95 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:161577 )

• all mice die by 17 months of age

neoplasm

increased gastrointestinal tumor incidence ( J:161577 )

• 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

increased small intestine adenocarcinoma incidence ( J:161577 )

• 50% of small intestine tumors are highly invasive adenocarcinomas

increased intestinal adenoma incidence ( J:161577 )

• 50% of small intestine tumors are adenomas

increased lymphoma incidence ( J:161577 )

• in only 1 of 150 mice

homeostasis/metabolism

abnormal mismatch repair ( J:161577 )

• 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

abnormal mismatch repair ( J:161577 )

• 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

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:161577 )

• 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

increased small intestine adenocarcinoma incidence ( J:161577 )

• 50% of small intestine tumors are highly invasive adenocarcinomas

increased intestinal adenoma incidence ( J:161577 )

• 50% of small intestine tumors are adenomas

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

Allelic Composition	Arnt^tm1.1Gonz/Arnt^tm1.1Gonz 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:
Arnt^tm1.1Gonz mutation (0 available); any Arnt mutation (65 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

hematopoietic system

decreased erythrocyte cell number ( J:189504 )

decreased hematocrit ( J:189504 )

decreased hemoglobin content ( J:189504 )

homeostasis/metabolism

decreased circulating iron level ( J:189504 )

Allelic Composition	Cdhr2^{tm1c(EUCOMM)Hmgu}/Cdhr2^{tm1c(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:
Cdhr2^{tm1c(EUCOMM)Hmgu} mutation (0 available); any Cdhr2 mutation (61 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

decreased body weight ( J:273165 )

• at P90, body weight is significantly lower than that of wild-type controls

postnatal growth retardation ( J:273165 )

• growth begins to lag behind that of wild-type controls in the second month of life into adulthood

digestive/alimentary system

abnormal intestinal epithelium morphology ( J:273165 )

• 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

abnormal enterocyte morphology ( J:273165 )

• enterocytes exhibit a domed apical surface with an abnormal outward/convex curvature

• however, apical-basolateral polarity and simple columnar morphology remain normal

abnormal duodenum crypts of Lieberkuhn morphology ( J:273165 )

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

abnormal jejunum morphology ( J:273165 )

• TEM of the brush borders in jejunal tissues revealed that enterocytes show prominent apical doming

abnormal small intestinal microvillus morphology ( J:273165 )

• 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

decreased small intestinal villus height ( J:273165 )

• mean villus length at the proximal (duodenal) end of the small intestine is significantly decreased

abnormal enterocyte physiology ( J:273165 )

• levels of key apical enzymes and transporters that are critical for enterocyte function are significantly reduced in the brush border

endocrine/exocrine glands

abnormal duodenum crypts of Lieberkuhn morphology ( J:273165 )

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

Allelic Composition	St18^{tm1c(KOMP)Wtsi}/St18^{tm1c(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:
St18^{tm1c(KOMP)Wtsi} mutation (0 available); any St18 mutation (71 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

growth/size/body region phenotype ( J:298828 )

N	• normal susceptibility to weight loss after oral DSS administration

mortality/aging

mortality/aging ( J:298828 )

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

Allelic Composition	Btnl6^em1Ahay/Btnl6^em1Ahay Tg(Vil1-cre)20Syr/0
Genetic Background	involves: C57BL/6 * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Btnl6^em1Ahay mutation (0 available); any Btnl6 mutation (25 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

hematopoietic system

decreased CD4-positive, gamma-delta intraepithelial T cell number ( J:291989 )

• in the gut

immune system

decreased CD4-positive, gamma-delta intraepithelial T cell number ( J:291989 )

• in the gut

Allelic Composition	Tg(Vil1-cre)20Syr/0 Vmp1^tm1.1Arte/Vmp1^tm1.1Arte
Genetic Background	involves: C57BL/6 * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Vil1-cre)20Syr mutation (4 available)
Vmp1^tm1.1Arte mutation (1 available); any Vmp1 mutation (38 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

digestive/alimentary system

abnormal enterocyte morphology ( J:280741 )

• accumulation of neutral lipids in intestinal epithelia at 8 months of age

growth/size/body

decreased body weight ( J:280741 )

• at 7 to 10 months of age

homeostasis/metabolism

abnormal lipid level ( J:280741 )

• accumulation of neutral lipids in intestinal epithelia at 8 months of age

• however, serum cholesterol and lipoproteins levels are normal

Allelic Composition	Apc^tm1Tyj/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:
Apc^tm1Tyj mutation (1 available); any Apc mutation (158 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased intestinal adenoma incidence ( J:160399 )

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

increased colon adenoma incidence ( J:160399 )

• develop by 4 - 5 months of age

digestive/alimentary system

increased intestinal adenoma incidence ( J:160399 )

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

increased colon adenoma incidence ( J:160399 )

• develop by 4 - 5 months of age

Allelic Composition	Lrp5^tm2Kry/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:
Lrp5^tm2Kry mutation (0 available); any Lrp5 mutation (82 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

skeleton

decreased bone mass ( J:146078 )

decreased bone ossification ( J:146078 )

• decreased bone formation

Allelic Composition	Lrp5^{tm3(Lrp5)Kry}/Lrp5^{tm3(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:
Lrp5^{tm3(Lrp5*)Kry} mutation (0 available); any Lrp5 mutation (82 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

decreased serotonin level ( J:146078 )

• decreased circulating serotonin levels

skeleton

increased bone mass ( J:146078 )

increased bone ossification ( J:146078 )

• increased bone formation

Allelic Composition	Znhit1^tm1.1Nju/Znhit1^tm1.1Nju 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 (4 available)
Znhit1^tm1.1Nju mutation (0 available); any Znhit1 mutation (16 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

postnatal lethality, incomplete penetrance ( J:276456 )

• some mice die following the first week after birth

digestive/alimentary system

abnormal crypts of Lieberkuhn morphology ( J:276456 )

• enlarged postnatally that fail to form intestinal organoids in vitro

• however, embryonic intestinal development is normal

increased Paneth cell number ( J:276456 )

abnormal small intestinal villus morphology ( J:276456 )

• at P9

growth/size/body

decreased body weight ( J:276456 )

• from P5 through P30

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:276456 )

• enlarged postnatally that fail to form intestinal organoids in vitro

• however, embryonic intestinal development is normal

increased Paneth cell number ( J:276456 )

Allelic Composition	Nras^tm1Tyj/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:
Nras^tm1Tyj mutation (1 available); any Nras mutation (44 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

decreased physiological sensitivity to xenobiotic ( J:132357 )

• 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

Allelic Composition	Rprd1b^tm1Tshu/Rprd1b^tm1Tshu Tg(Vil1-cre)20Syr/0
Genetic Background	involves: C57BL/6 * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rprd1b^tm1Tshu mutation (0 available); any Rprd1b mutation (16 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

increased susceptibility to colitis induced morbidity/mortality ( J:300857 )

• all DSS treated mice unlike similarly treated control mice

prenatal lethality, incomplete penetrance ( J:300857 )

• fewer than expected mice are born

digestive/alimentary system

digestive/alimentary phenotype ( J:300857 )

N	• mice exhibit normal villus number and structure in the small intestine

abnormal small intestine goblet cell morphology ( J:300857 )

• reduced number

abnormal digestive system development ( J:300857 )

• impaired proliferation and differentiation of Lgr5+ stem cells

abnormal large intestine crypts of Lieberkuhn morphology ( J:300857 )

• enlarged and thickened

abnormal large intestine goblet cell morphology ( J:300857 )

• reduced number

decreased Paneth cell number ( J:300857 )

• fewer lysozyme positive Paneth cells

impaired intestine regeneration ( J:300857 )

• failure to regenerated colon crypts after X-ray damage

increased susceptibility to colitis induced morbidity/mortality ( J:300857 )

• all DSS treated mice unlike similarly treated control mice

growth/size/body

decreased body weight ( J:300857 )

• in surviving mice

homeostasis/metabolism

impaired wound healing ( J:300857 )

• failure to regenerated colon crypts after X-ray damage

immune system

increased susceptibility to colitis induced morbidity/mortality ( J:300857 )

• all DSS treated mice unlike similarly treated control mice

cellular

abnormal large intestine goblet cell morphology ( J:300857 )

• reduced number

abnormal small intestine goblet cell morphology ( J:300857 )

• reduced number

endocrine/exocrine glands

abnormal large intestine crypts of Lieberkuhn morphology ( J:300857 )

• enlarged and thickened

abnormal large intestine goblet cell morphology ( J:300857 )

• reduced number

decreased Paneth cell number ( J:300857 )

• fewer lysozyme positive Paneth cells

Allelic Composition	Tph1^tm1Kry/Tph1^tm1Kry 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 (4 available)
Tph1^tm1Kry mutation (0 available); any Tph1 mutation (41 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cellular

increased osteoblast proliferation ( J:146078 )

• increased osteoblast proliferation

homeostasis/metabolism

decreased serotonin level ( J:146078 )

• decreased circulating serotonin levels

skeleton

increased osteoblast proliferation ( J:146078 )

• increased osteoblast proliferation

increased osteoblast cell number ( J:146078 )

increased bone mass ( J:146078 )

• severe

• ovariectomy does not result in decreased bone mass unlike in controls

increased bone ossification ( J:146078 )

• increased bone formation

Allelic Composition	Lrp5^tm2Kry/Lrp5^tm2Kry Tg(Vil1-cre)20Syr/0
Genetic Background	involves: C57BL/6 * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lrp5^tm2Kry mutation (0 available); any Lrp5 mutation (82 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cellular

decreased osteoblast proliferation ( J:146078 )

• decreased osteoblast proliferation

homeostasis/metabolism

abnormal serotonin level ( J:146078 )

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

skeleton

decreased osteoblast proliferation ( J:146078 )

• decreased osteoblast proliferation

decreased osteoblast cell number ( J:146078 )

decreased bone mass ( J:146078 )

decreased bone ossification ( J:146078 )

• decreased bone formation

vision/eye

vision/eye phenotype ( J:146078 )

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

Allelic Composition	Gt(ROSA)26Sor^{tm2(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)26Sor^{tm2(sb11)Njen} mutation (7 available); any Gt(ROSA)26Sor mutation (993 available)
TgTn(sb-T2/Onc)68Dla mutation (1 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:146887 )

neoplasm

increased gastrointestinal tumor incidence ( J:146887 )

• increased incidence of intraepithelial neoplasias in the small and large intestines

increased small intestine adenocarcinoma incidence ( J:146887 )

increased intestinal adenoma incidence ( J:146887 )

• adenomas are seen in the small and large intestines

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:146887 )

• increased incidence of intraepithelial neoplasias in the small and large intestines

increased small intestine adenocarcinoma incidence ( J:146887 )

increased intestinal adenoma incidence ( J:146887 )

• adenomas are seen in the small and large intestines

Allelic Composition	Gt(ROSA)26Sor^{tm2(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)26Sor^{tm2(sb11)Njen} mutation (7 available); any Gt(ROSA)26Sor mutation (993 available)
TgTn(sb-T2/Onc)76Dla mutation (1 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:146887 )

neoplasm

increased gastrointestinal tumor incidence ( J:146887 )

• increased incidence of intraepithelial neoplasias in the small and large intestines

increased small intestine adenocarcinoma incidence ( J:146887 )

increased intestinal adenoma incidence ( J:146887 )

• adenomas are seen in the small and large intestines

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:146887 )

• increased incidence of intraepithelial neoplasias in the small and large intestines

increased small intestine adenocarcinoma incidence ( J:146887 )

increased intestinal adenoma incidence ( J:146887 )

• adenomas are seen in the small and large intestines

Allelic Composition	Cep55^{tm1c(EUCOMM)Hmgu}/Cep55^{tm1c(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:
Cep55^{tm1c(EUCOMM)Hmgu} mutation (0 available); any Cep55 mutation (71 available)
Tg(Vil1-cre)20Syr mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

digestive/alimentary system

digestive/alimentary phenotype ( J:287102 )

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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