Corticosteroid-induced cleft palate in mice and H-2 haplotype: maternal and embryonic effects.
This report confirms and expands on the original preliminary observations made by Bonner and Slavkin that corticosteroid-induced cleft palate in mice is associated with H-2 haplotype. Using three congenic strains, B10, B10.A, and B10.D2, our studies demonstrate that B10.A (H-2a) is most susceptible and B10.D2(H-2d) is least susceptible, B10(H-2b) being intermediate. Variation in fetal loss among strains accounts for less than 1 percent of the variation in cleft-palate frequency among strains; variation in H-2 haplotype, however, accounts for more than 60 percent of the variation in cleft-palate frequency. With regard to all possible reciprocal F1 hybrids, our results indicate that while there is a significant maternal effect, maternal haplotype can account for only 11 percent of the variation in cleft-palate frequency among crosses. Embryonic haplotype accounts for 17 percent of the variation, which is indicative of an important embryonic effect. Finally, our studies suggest that susceptibility to corticosteroid-induced cleft palate is associated with the K end of the H-2 complex.
D000305:Adrenal Cortex Hormones / Q000009:adverse effects; D000818:Animals; D002972:Cleft Palate / Q000139:chemically induced* / Q000235:genetics*; D003433:Crosses, Genetic; D005260:Female; D005313:Fetal Death; D014644:Genetic Variation; D006183:H-2 Antigens / Q000235:genetics*; D051379:Mice; D008810:Mice, Inbred C57BL / Q000235:genetics; D010641:Phenotype; D011247:Pregnancy; D013045:Species Specificity
D000305:Adrenal Cortex Hormones; D006183:H-2 Antigens