Abstract
The purpose of this study was to detect genetic factors affecting the appearance of cleft palate induced cortisone using genetic crosses between A/WySn and C 3 H/He mice. Embryos From withinstrain breeding of A/WySn and C 3/He, and the F1 intercross and N2 backcross embryos from crosses between the two strains were used to evaluate cortisone susceptibility. On day 11 to 14 gestation, the mice were given subcutaneous injections of cortisone acetate. On day 18 the embryos were dissected for observation of cleft palate. The frequency of cleft palate in the A/WySn strain treated with cortisone was 65.4%, on the other hand 12.1% in the C 3 H/He mice. The frequency in F1 mice was significantly lower compare with that in the A/WySn strain, indicating recessive transmission. To investigate the influence of an X-linked factor, we judged the sexuality of N2 embryos using polymerase chain reaction (PCR). There was no significant difference in the incidence between the sexes among N2 mice. These findings suggest the cortisone-induced cleft palate in mice was influenced by major gene effect with autosomal recessive transmission. Genetic maternal effect in the appearance of cleft palate was not detected in this study. The significant difference between the two strains in the incidence of cleft palate indicates that mapping of susceptibility loci for cortisone would be possible using linkage analysis. To evaluate a linkage between the gene responsible for cleft palate inducing cortisone and H-2 region on chromosome 17, which have been associated with cortisone susceptibility, we performed the genotyping of the individual N2 with cleft palate using MIT primer located in the H-2 region. The genotyping results suggested that the H-2 S region might be associated with cortisone susceptibility in the occurrence of cleft palate.
