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Genome-wide association studies have revealed that many low-penetrance cancer susceptibility loci are located throughout the genome; however, a very limited number of genes have been identified so far. Using a forward genetics approach to map such loci in a mouse skin cancer model, we previously identified strong genetic loci conferring resistance to early-stage chemically induced skin papillomas on chromosome 7 with a large number of [(FVB/N×MSM/Ms)×FVB/N] F1 backcross mice. In this report, we describe a combination of congenic mapping and allele-specific alteration analysis of the loci on chromosome 7. We used linkage analysis and congenic mouse strains to refine the location of  Stmm1  (  S kin  t umor  m odifier of  M SM  1  ) locus within a genetic interval of about 3 cM on proximal chromosome 7. In addition, we used patterns of allele-specific imbalances in tumors from F1 backcross and N10 congenic mice to narrow down further the region of  Stmm1  locus to a physical distance of about 5.4 Mb. To gain the insight into the function of  Stmm1  locus, we carried out a long term BrdU labelling experiments with congenic mice containing  Stmm1  locus. Interestingly, we observed a decrease of BrdU-LRCs ( L abel  R etaining  C ells) in a congenic strain heterozygous or homozygous for MSM allele of  Stmm1 . These results suggest that  Stmm1  responsible genes may have an influence on papillomagenesis in the two-stage skin carcinogenesis by regulating epidermal quiescent stem cells.

Congenic Mapping and Allele-Specific Alteration Analysis of Stmm1 Locus Conferring Resistance to Early-Stage Chemically Induced Skin Papillomas