Genetics of cortisone-induced cleft palate in the mouse-embryonic and maternal effects.
Differences between mouse strains in frequency of embryonic, cortisone-induced cleft palate were examined. Probit analysis demonstrated a family of linear and parallel dose-response curves for different inbred and hybrid embryos. Since the differences between genotypes were not in the slopes of the response curves but rather in their location, it is proposed that the median effective dose (ED50) of cortisone required to induce cleft palate (or the tolerance) provides a more appropriate definition of the response trait and its difference that a frequency statement. The tolerance of C57BL/6J is dominant to that of A/J. A maternal effect of A/J relative to C57BL/6J dams caused a two-fold reduction in the embryonic tolerance of cortisone. Cortisone-induced cleft palate and mortality were separate response traits. In these and previous studies on cortisone- and other glucocorticoid-induced cleft palate in the mouse, the nature of the cleft-palate-response curve appeared to be the same for all glucocorticoids, and within-strain differences in tolerance could be used as measures of potency or bioassays for a particular effect of the glucocorticoids.
D000818:Animals; D002972:Cleft Palate / Q000235:genetics*; D003348:Cortisone / Q000494:pharmacology*; D003433:Crosses, Genetic; D004305:Dose-Response Relationship, Drug; D005260:Female; D005796:Genes; D005838:Genotype; D005938:Glucocorticoids / Q000494:pharmacology; D008297:Male; D051379:Mice; D008805:Mice, Inbred A; D008810:Mice, Inbred C57BL; D013045:Species Specificity; D013223:Statistics as Topic; D013723:Teratogens; D013997:Time Factors
D005938:Glucocorticoids; D013723:Teratogens; D003348:Cortisone