H-2 and non-H-2 determined strain variation in palatal shelf and tongue adenosine 3':5' cyclic monophosphate: a possible role in the etiology of steroid-induced cleft palate.

The concentration of cAMP was measured in palatal shelves and tongues of 14.5-day old foetuses, 14.5-day old foetuses from steroid treated mothers, and 15.5-day old foetuses from four inbred lines of mice which represent the four possible combinations of two H-2 alleles and two residual genetic backgrounds. The incidence of spontaneous and steroid-induced cleft palate in these four strains was also determined. Analyses of variance of the cAMP data reveal that both the H-2 region and residual genetic background determine cAMP concentrations in both tissues and on both days of development. Similar analyses of cAMP concentrations after steroid treatments of the mother indicate that the interaction between H-2 and residual genetic background is significantly different in the injected than in the uninjected mice in both palatal shelves and tongues. The incidence of steroid-induced cleft palate parallels the palatal shelf concentration of cAMP before steroid treatment of the mother with one exception. These data suggest that a portion of the H-2 controlled component of susceptibility to steroid-induced cleft palate is mediated through alterations in the metabolism of cAMP.