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Abstract
Abstract The genetic effects of the H‐2 histocompatibility gene complex on the frequencies of urethan and ethylnitrosourea (ENU)‐induced malformations in prenatal fetuses of mice were examined, and a new functional gene linked to the H‐2 complex on chromosome 17 was mapped.The H‐2 congenic pair strains of mouse, BIO.A and C57BL/10 (BIO), were tested for susceptibility to urethan‐induced external malformations in fetuses. The BIO.A strain expressing the H‐2a haplotype characteristically showed a high susceptibility to urethan‐induced Polydactyly and kinky tail. However, the BIO strain expressing the H‐2b haplotype was resistant to urethan‐induced malformation. The same tendency was observed for ENU‐induced malformations. Thus, susceptibilities to urethan and ENU‐induced external malformation must be affected by a gene linked to the H‐2 complex.In a mapping study using BIO.A recombinant mouse strains, BIO.A (5R) was sensitive, while BIO.A (2R) and B10.A (4R) were resistant to urethan‐induced external malformations. Variations in the susceptibility to teratogenicity of urethan in BIO.A recombinant strains indicated that a new functional gene located between the H‐2 S region and the Upg‐1 locus on chromosome 17 was involved in regulation of susceptibility.
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