PubMed1983
Around 60% of mice homozygous for the curly-tail gene have neural tube defects (NTD). F1 hybrids between curly-tail mice (ct) and a nongenetically predisposed A strain (A) do not have NTD. Vitamin A increases the penetrance of the ct gene at doses that hardly cause any NTD in A mice. The susceptibility to vitamin A of the F1 hybrids, derived from ct female X A male and A female X ct male crosses, was examined. Either 10, 20, or 40 mg/kg was injected into the mother on the eighth day of pregnancy. The F1 hybrids did develop NTD, and there was a dose response. The number with NTD was roughly intermediate between that found in the two pure parental crosses. However, there was a significant difference in response according to whether the ct or the A was the mother, more F1 embryos having NTD in the former situation. Also, significantly more of the female F1 hybrids had NTD when the ct was the mother than when the A was the mother, but for the males, the number with NTD was the same in both crosses. The number of intrauterine deaths of F1 hybrids, seen as resorptions in each reciprocal cross, was not intermediate but matched that of the pure parental strain of the mother involved in the hybrid cross. It is concluded that gene-environment interaction has been demonstrated, together with both a maternal effect and a contribution of the fetal genotype in the liability to produce NTD in response to vitamin A.