Phenotypes associated with this allele

• Allele Symbol: Gpa33^tm1Jkhh
• Allele Name: targeted mutation 1, Joan K Heath
• Allele ID: MGI:5774782
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Gpa33^tm1Jkhh/Gpa33^tm1Jkhh	B6.129-Gpa33^tm1Jkhh	MGI:5775163
hm2	Gpa33^tm1Jkhh/Gpa33^tm1Jkhh	involves: 129 * C57BL/6	MGI:5775164

Genotype
MGI:5775163

hm1

• Allelic Composition: Gpa33^tm1Jkhh/Gpa33^tm1Jkhh
• Genetic Background: B6.129-Gpa33^tm1Jkhh

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

immune system

increased susceptibility to induced colitis ( J:224768 )

• DSS-treated mice exhibit more rapid colitis onset and increased colitis score compared with wild-type mice

• DSS-treated mice exhibit increased susceptibility to chronic colitis with more exaggerated weight loss, impaired crypt regeneration and resolution of colonic inflammation compared with wild-type mice

• however, severity of colitis is normal

increased dendritic cell number ( J:224768 )

• in colonic lamina prioria, especially activated dendritic cells and activated CD103+ gut-resident dendritic cells

• however, spleen numbers are normal

increased susceptibility to type IV hypersensitivity reaction ( J:224768 )

• to oral ovalbumin with broken oral tolerance

abnormal immune tolerance ( J:224768 )

• impaired oral tolerance to ovalbumin

digestive/alimentary system

digestive/alimentary phenotype ( J:224768 )

N • mice exhibit normal intestinal epithelial cell lineage differentiation and proliferation in addition to an extremely mild, age-progressive colitis without steady-state colitis

abnormal intestinal epithelium physiology ( J:224768 )

• impaired intestinal barrier functions after DSS treatment

• however, untreated mice exhibit normal intestinal barrier function

increased susceptibility to induced colitis ( J:224768 )

• DSS-treated mice exhibit more rapid colitis onset and increased colitis score compared with wild-type mice

• DSS-treated mice exhibit increased susceptibility to chronic colitis with more exaggerated weight loss, impaired crypt regeneration and resolution of colonic inflammation compared with wild-type mice

• however, severity of colitis is normal

neoplasm

increased incidence of tumors by chemical induction ( J:224768 )

• AOM/DSS-treated mice exhibit increased colon tumor burden compared with wild-type mice

• however, mice are not predisposed to sporadic colorectal cancer

growth/size/body

increased susceptibility to weight loss ( J:224768 )

• in mice chronically-treated with DSS

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:224768 )

• AOM/DSS-treated mice exhibit increased colon tumor burden compared with wild-type mice

• however, mice are not predisposed to sporadic colorectal cancer

hematopoietic system

increased dendritic cell number ( J:224768 )

• in colonic lamina prioria, especially activated dendritic cells and activated CD103+ gut-resident dendritic cells

• however, spleen numbers are normal

Genotype
MGI:5775164

hm2

• Allelic Composition: Gpa33^tm1Jkhh/Gpa33^tm1Jkhh
• Genetic Background: involves: 129 * C57BL/6

mortality/aging

increased susceptibility to colitis induced morbidity/mortality ( J:231808 )

• with colonic perforation in TNBS-treated mice

digestive/alimentary system

diarrhea ( J:231808 )

• in TNBS-treated mice

abnormal intestine morphology ( J:231808 )

• bowel wall thickening in TNBS-treated mice

abnormal large intestine crypts of Lieberkuhn morphology ( J:231808 )

• in TNBS-treated mice

• 10-fold increase in crypt fission following induction of colitis

decreased colon goblet cell number ( J:231808 )

• in TNBS-treated mice

decreased intestinal mucosa thickness ( J:231808 )

• in untreated mice

intestinal ulcer ( J:231808 )

• small areas of mild focal ulceration in untreated mice

• ulceration in TNBS-treated mice

abnormal intestinal epithelium physiology ( J:231808 )

• TNBS-treated mice exhibit slightly delayed proliferative response in colonic crypts compared with wild-type mice

• however, the long-term number of crypt cells is normal

increased susceptibility to induced colitis ( J:231808 )

• mice treated with TNBS exhibit ulceration, inflammation, bowel wall thickening, diarrhea and increased mortality with increased severity and delayed healing response compared with wild-type mice

increased susceptibility to colitis induced morbidity/mortality ( J:231808 )

• with colonic perforation in TNBS-treated mice

immune system

increased susceptibility to induced colitis ( J:231808 )

• mice treated with TNBS exhibit ulceration, inflammation, bowel wall thickening, diarrhea and increased mortality with increased severity and delayed healing response compared with wild-type mice

increased susceptibility to colitis induced morbidity/mortality ( J:231808 )

• with colonic perforation in TNBS-treated mice

homeostasis/metabolism

impaired wound healing ( J:231808 )

• in the colons of TNBS-treated mice

endocrine/exocrine glands

abnormal large intestine crypts of Lieberkuhn morphology ( J:231808 )

• in TNBS-treated mice

• 10-fold increase in crypt fission following induction of colitis

decreased colon goblet cell number ( J:231808 )

• in TNBS-treated mice

cellular

decreased colon goblet cell number ( J:231808 )

• in TNBS-treated mice