| First Author | Dove W | Year | 1995 |
| Journal | 9th International Mouse Genome Conference | Pages | 27 (Abstr. 15) |
| Mgi Jnum | J:30726 | Mgi Id | MGI:78288 |
| Citation | Dove W, et al. (1995) Second-site genetic analysis of multiple intestinal neoplasia. 9th International Mouse Genome Conference :27 (Abstr. 15) |
| abstractText | Full text of Abstract: 15. SECOND-SITE GENETIC ANALYSIS OF MULTIPLE INTESTINAL NEOPLASIA. W. Dove, K. Gould, D. Katzung, C. Luongo, A. Moser, A. Shoemaker (McArdle Laboratory, University of Wisconsin); L. Donehower (Baylor College of Medicine); K. Hong, W. Dietrich, E. Lander (Whitehead Institute, MIT). A common strategy to identify genetic networks is to screen for alleles at secondary loci that modify the phenotype caused by a mutation at a primary effector locus. Mom-1 modifies the multiplicity of intestinal adenomas in mice heterozygous for the Min allele of the Apc locus. Analysis of Mom-1 homozygotes and heterozygotes indicate that Mom-1 acts in semi-dominant fashion. MacPhee and her collaborators (CELL 81:957, 1995) have proposed that resistance alleles of Mom-1 encode the secretory type 11 phospholipase (Pla2s) and that sensitivity alleles fail to express this enzyme. Candidates in the region of Mom-1 including Pla2s are being tested. Is Mom-1 the only polymorphic modifier locus for Min? The strain AKR carries more than one modifier locus; when Min is congenic on the AKR background, the tumor multiplicity is less than 1.0 for the entire intestinal tract. To expand the set of Mom loci, one must look beyond polymorphisms to mutant alleles including those that are homozygous lethal. Heterozygotes for dnmt, a recessive lethal deficiency in DNA cytosine maintenance methylase, develop a reduced number of Min-induced adenomas (Laird et al., CELL 81:197, 1995). Modification of the phenotype of Min/+ animals by a null allele of p53 will be discussed. |
