Cortisone-induced cleft palate in the mouse. A search for the genetic control of the embryonic response trait.
The cause of the difference in the mean tolerance (ED50) to cortisone-induced cleft palate between the embryos of the A/J and C57BL/6J strains appears to be due to a small number of genes. A single major gene effect and a polygenic model, in the sense of many equal and additive genes, have been ruled out. The embryonic tolerance of C57BL/6J  is greater than and dominant to that of A/J; two or three loci, possibly with independent effects, appear to explain the variability. A component of the variation in embryonic response may be associated with or linked to the major histocompatibility locus (H-2). No evidence was found to support the hypothesis of X-chromosome linked susceptibility to cortisone-induced cleft palate.
D000014:Abnormalities, Drug-Induced / Q000235:genetics*; D000818:Animals; D002874:Chromosome Mapping; D002972:Cleft Palate / Q000139:chemically induced* / Q000235:genetics; D003348:Cortisone; D005260:Female; D005796:Genes / Q000187:drug effects*; D008040:Genetic Linkage; D014644:Genetic Variation; D005838:Genotype; D006680:HLA Antigens; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D011336:Probability; D012730:Sex Chromosomes
D006680:HLA Antigens; D003348:Cortisone