| First Author | Koratkar R | Year | 2004 |
| Journal | Genomics | Volume | 84 |
| Issue | 5 | Pages | 844-52 |
| PubMed ID | 15475263 | Mgi Jnum | J:93365 |
| Mgi Id | MGI:3056946 | Doi | 10.1016/j.ygeno.2004.07.010 |
| Citation | Koratkar R, et al. (2004) Analysis of reciprocal congenic lines reveals the C3H/HeJ genome to be highly resistant to Apc(Min) intestinal tumorigenesis. Genomics 84(5):844-52 |
| abstractText | Genetic background affects polyp development in the Multiple intestinal neoplasia (Apc(Min)) mouse model. The Modifier of Min 1 (Mom1) locus accounts for ~50% of the variation in polyp multiplicity. We generated reciprocal congenic lines, such that the recipient C57BL/6J (B6) strain carries a donor C3H/HeJ (C3H) Mom1 allele, and the recipient C3H strain carries a donor B6 Mom1 allele. Hybrid progeny from congenic females mated to B6 Apc(Min/+) males were analyzed. A single C3H Mom1 locus on the B6 background reduced small intestinal polyp numbers by 50% and colon polyp incidence by 66% compared to their susceptible B6 Mom1(S/S)Apc(Min/+) siblings. These findings show that the C3H genome contains a resistant Mom1(R) locus. The reciprocal congenic line, which carries the susceptible B6 Mom1(S) locus on the C3H background, reduced small intestinal polyp numbers by 80% and colon polyp incidence by 95% compared to B6 Mom1(S/S)Apc(Min/+) mice. These data demonstrate that unidentified modifiers in the C3H strain can suppress intestinal polyp multiplicity in Apc(Min/+) mice, and act in the absence of a resistant Mom1(R) locus. |
