Heterozygotes of this strain develop anemia and are highly susceptible to spontaneous intestinal adenoma formation. Homozygous C57BL/6J-ApcMin/J mice are not viable. The increased incidence of colorectal adenomas renders these mice a useful model of colon cancer. A small number of C57BL/6J-ApcMin heterozygous female mice develop mammary tumors.
Dr. Alexandra Shedlovsky, University of Wisconsin , Madison
Dr. William F. Dove, University of Wisconsin- Madison
The C57BL/6J-ApcMin/J strain is highly susceptible to spontaneous intestinal adenoma formation. Homozygous mice are not viable. It was initially reported that one hundred percent of the C57BL/6J-ApcMin heterozygous mice raised on a high fat diet develop in excess of 30 adenomas throughout the intestinal tract and most die by 120 days of age. Heterozygotes also develop anemia. (Moser et al., 1990, Su et al., 1992). A small number of C57BL/6J-ApcMin heterozygous female mice develop mammary tumors. A subsequent publication indicates that this strain may carry a dominant modifier (Mom2) gene that reduces the number and incidence of polyp formation in C57BL/6J-ApcMin heterozygous mice (Silverman et al., 2002).
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Following N-ethyl-N-nitrosourea (ENU) treatments to induce mutations in founder C57BL/6J mice, a forward genetic screen identified a AKR/JxB6 F1 female displaying circling behavior. This female was mated to C57BL/6J males. Some progeny from this backcross developed adult onset anemia and multiple intestinal neoplasia (Min). A tumor suppressor gene, Apc (adenomatosis polyposis coli), mutations of which have been identified in colorectal cancers and familial adenomatous polyposis (FAP), was found to cosegregate with the Min phenotype. Sequencing of Apc identified a T to A transversion of nucleotide 2549 resulting in a Leucine to a Stop codon nonsense mutation. The circling behavior was determined to be a separate heritable trait and was eliminated through subsequent crosses to C57BL/6J. These ApcMin mice maintained on a C57BL/6J background when they were sent to The Jackson Laboratory in 1992.
|Allele Name||multiple intestinal neoplasia|
|Allele Type||Chemically induced (ENU)|
|Allele Synonym(s)||multiple intestinal neoplasia; ApcMin|
|Gene Symbol and Name||Apc, adenomatosis polyposis coli|
|Gene Synonym(s)||RATAPC; DP2; DP3; expressed sequence AW124434; Min; Min; BTPS2; AU020952; expressed sequence AI047805; CC1; GS; PPP1R46; multiple intestinal neoplasia; expressed sequence AU020952; DP2.5; AI047805; AW124434; adenomatosis polyposis coli; DESMD|
|Strain of Origin||C57BL/6J|
|Molecular Note||A transversion point mutation that alters nucleotide 2549 from a T to an A (mRNA: NM_001360980.1; protein: NM_007462.3). This converts codon 850 from one encoding a leucine to a stop codon (p.Leu850*), truncating the expected polypeptide.|
|Mutations Made By|| |
Dr. William Dove, University of Wisconsin- Madison
This strain is maintained by breeding heterozygote males to C57BL/6J females. Female heterozygotes are not recommended because anemia and intestinal adenomas interfere with pregnancy. Breeding performance in heterozygote males declines as anemia and tumors develop.
When using the multiple intestinal neoplasia mouse strain in a publication, please cite the originating article(s) and include JAX stock #002020 in your Materials and Methods section.
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