Genetics of clefting in the mouse

Abstract

Whether the relative sensitivity of A/J to CP induction by many teratogens is due to a common mechanism has not been explored beyond cortisone and 6-AN. These latter were found to be probably independent systems. For 6-NA it was suggested that the strain difference was due to three loci with dominance and epistasis and acting in embryos, so that relative liability like that shown by A/J would be derived from simultaneous homozygosity for recessive genes at three loci. The strain difference in CP response to cortisone was explained by two loci with dominance, but with independent effects (no epistasis), and a maternal effect. At least part of the maternal effect and one of the embryonic loci were associated with the H-2 complex.