Genetics of cleft palate in chickens and the relationship between the occurrence of the trait and maternal riboflavin deficiency.

Reciprocal crosses were made between a New Hampshire line of chickens free of cleft palate and affected individuals of a highly inbred S.C.W. Leghorn line having 30 to 50% incidence of cleft palate. The frequency of cleft palate was observed under normal and riboflavin deficient maternal nutrition for the reciprocals of the F1, F2, and backcross to the cleft palate line. Two cases of cleft palate were found in dead embryos of 1368 F1 observations. These may not have represented the genetic trait under study. The response of egg hatchability to riboflavin deficiency was shown to be earlier for cleft palate line hens than for F1 hens, but no maternal effects were found for cleft palate incidence. The frequency of cleft palate in the F2 increased from 0.7% during normal maternal nutrition, to 4.4% during maternal riboflavin deficiency. A similar increase from 8.0% to 12.4% was seen in the backcross progeny. The cleft palate trait was found to be semi-lethal, with mortality associated with severe expression of the trait. No significant sex differences in cleft palate incidence was found in the F2 or backcross generations. The F2 and backcross cleft palate data fit models of genetic control by 3 recessive loci during normal maternal nutrition, and 2 recessive loci during maternal riboflavin deficiency. Penetrance was indicated to be under additive genetic control, and the average was calculated to be between 50 and 75% for all cases. The loss of relevance of one locus during maternal riboflavin deficiency was interpreted to indicate that the homozygous recessive condition at that locus gave disturbed riboflavin metabolism. It was further interpreted to explain the increased occurrence of some traits during teratogenic circumstances as due to the increased probability of obtaining recessive homozygosity at (n - 1) loci compared to (n) loci, and that the role of teratogens in some traits may be in mimicking specific genetic components of the traits.