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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Foxl1tm1Khk
targeted mutation 1, Klaus H Kaestner
MGI:2178230
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Foxl1tm1Khk/Foxl1tm1Khk involves: 129P2/OlaHsd * C57BL/6 MGI:3834879
cx2
ApcMin/Apc+
Foxl1tm1Khk/Foxl1tm1Khk
involves: 129P2/OlaHsd * C57BL/6 MGI:3834880


Genotype
MGI:3834879
hm1
Allelic
Composition
Foxl1tm1Khk/Foxl1tm1Khk
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxl1tm1Khk mutation (0 available); any Foxl1 mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mice die prior to weaning, typically between 1 and 3 weeks of age

growth/size/body
• weight is normal at birth but surviving mutants show marked growth retardation; after weaning, survivors display rapid weight gain and reach size of normal littermates by about 5 months

digestive/alimentary system
• goblet cells are found clustered in within the crypts as well as in the villi in increased number in the duodenum and jejunum in contrast to normal littermates where goblet cells are found distributed throughout the villus in an anterior-posterior gradient in the intestine
• at E14.5, intestinal mesenchyme has not started in invaginate to form epithelial ridges, causing delay in formation of villi; at E16.5 and E18.5, fewer, poorly-formed villi are present
• from E14.5 to 18.5, mesenchyme is less condensed than in normal littermates
• after E16.5, intervillus regions continue to contain stratified epithelium to a greater extent than in normal embryos
• at E18.5, proliferating cells are detected in intervillus region and scattered throughout the villi in contrast to wild-type where proliferating cells are found only in intervillus region of intestinal epithelium
• by P12, crypts appear to be expandeded and exhibit a branched morphology
• crypt compartment is expanded and disorganized by P50; abnormalities in crypt architecture are most noticeable in proximal intestine
• numbers of apoptotic cells in crypts are increased compared to controls at 50 days
• by postnatal day 3, jejunum of mutants has fewer villi than normal controls; villi are shorter and wider than controls
• numbers of apoptotic cells in crypts are increased compared to controls at 50 days
• at E18.5, villi are poorly formed, shorter and fewer in number compared to normal littermates
• by postnatal day 3, jejunum of mutants has fewer villi than normal controls; villi are shorter and wider than controls
• in animals >50 days of age, length of villi are increased compared to controls
• in 50 day-old animals, zone of proliferating cells is expanded corresponding to expanded crypt compartment; number of proliferating cells is increased by 4-fold compared to controls
• at E18.5, villi are shorter than in normal littermates
• by p3, vacuolization of surface cells and branching of glands within mucosa is observed
• subepithelial mesenchymal tissue is less dense and expanded compared to normal controls at P3; at day 50 submucosal mesenchyme is less condensed
• in adult animals, gastric mucosa is up to 6-fold thicker than normal; large cell-lined cysts and distorted mucosal glands are observed
• parietal cells show disorganized distribution while in normal controls, parietal cells are in orderly columns primarily within the isthmus and neck region of glandular epithelium
• staining for mucus cells in normal animals is strongly positive in gastric pit region but in mutants staining is strongly positive from the surface to the base of the glandular epithelium possibly to to migration of surface mucous cells throughout the gastric epithelium
• proliferating cell zone is markedly expanded throughout thickness of mucosa
• by P3, epithelium is expanded and structure is distorted

endocrine/exocrine glands
• by P12, crypts appear to be expandeded and exhibit a branched morphology
• crypt compartment is expanded and disorganized by P50; abnormalities in crypt architecture are most noticeable in proximal intestine
• numbers of apoptotic cells in crypts are increased compared to controls at 50 days

neoplasm
N
• no gastric adenomas are observed

cellular
• goblet cells are found clustered in within the crypts as well as in the villi in increased number in the duodenum and jejunum in contrast to normal littermates where goblet cells are found distributed throughout the villus in an anterior-posterior gradient in the intestine




Genotype
MGI:3834880
cx2
Allelic
Composition
ApcMin/Apc+
Foxl1tm1Khk/Foxl1tm1Khk
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (12 available); any Apc mutation (154 available)
Foxl1tm1Khk mutation (0 available); any Foxl1 mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• mutants do not show increased tumor multiplicity up to 90 days in the small intestine compared to heterozygous ApcMin mice
• adenomatous polyps contain a large number of proliferating epithelial cells
• no evidence of invasion or metastases are observed in any tumors in the colon

digestive/alimentary system
• mice develop a 7.7-fold higher number of colonic polyps compared to heterozygous ApcMin mice with wild-type Foxl1
• mice develop an average of 5.5 polyps in the stomach by 3 months of age, compared to no polyps in heterozygous ApcMin mice with wild-type Foxl1
• adenomatous polyps form in the stomach with disturbed glandular architecture and nuclear atypia; polyps contain large numbers of proliferating epithelial cells
• adenomatous polyps contain a large number of proliferating epithelial cells
• no evidence of invasion or metastases are observed in any tumors in the colon

cellular
• cells from adenomatous colonic polyps isolated from 30-day-old mice show loss of heterozygosity (LOH) of the wild-type Apc allele while colonic mucosa from heterozygous ApcMin mice show no LOH
• cells from gastric adenomas isolated from 30-day-old mice show >90% loss of heterozygosity (LOH) of the wild-type Apc allele similar to LOH observed in adenomas from 79-day-old heterozygous ApcMin mice





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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
05/07/2024
MGI 6.23
The Jackson Laboratory