Rats are an important experimental model for many human diseases, many of which have a genetic component. As followup of our previous and ongoing work demonstrating impressive differences in the phenotypic responses of LEW and F344 rats to proinflammatory and noninflammatory stimuli, we are developing a genetic linkage map for rats, specifically applicable to these rat strains. We have now identified 250 polymorphisms and have mapped about 200 of these to 17 of 20 rat chromosomes using an F2 intercross of F344 x LEW parents. We do not yet have markers for 3 rat chromsomes. We have demonstrated impressive conservation of synteny between rat, mouse and human chromosomes. We have also extended our efforts to identify polymorphisms to 13 additional inbred strains of rats. Importantly, we have identified approximately an additional 150 polymorphic markers that differ between the LEW and inbred BN rats, another relatively autoimmune disease resistant rat strain. In summary, we have markedly increased our ability to chromosomally localize genes that control important phenotypic traits in rats. Moreover, these markers are highly useful for genetic monitoring of inbred rat strains. As part of our effort to localize the athymic nude gene in the rat, we have genomically cloned, sequenced and mapped the rat epimorphin gene to chromosome 12 and have excluded it as a candidate locus for the rat athymic nude trait, which has been localized to chromosome 10.
