The International Complex Trait Consortium

C-Myc and Cdc25A are candidates for the mammary tumor latency modifier genes Apmt1 and Apmt2

Kent Hunter

Laboratory of Population Genetics CCR/NCI/NIH
Bldg 41 Rm 702 41 Library Drive Bethesda, MD 20892 USA

ABSTRACT
 
The epistatically interacting modifier loci (Apmt1 and Apmt2) accelerate the polyoma Middle-T (PyMT) induced mammary tumor. Using a bioinformatics strategy Cdc25A and c-Myc were identified as candidate genes. Molecular and in vitro analysis revealed functional differences for both genes between the mouse-inbred strains in question. Compound PyMT/Myc double transgenic animals were generated to mimic the hypothetical model and were found to recapitulate the age-of-onset phenotype. These data suggest that c-Myc and Cdc25A are Apmt1 and Apmt2, and suggest that at least in certain instances bioinformatics can be utilized to bypass congenic construction and subsequent mapping in conventional QTL studies.