The genetics and epigenetics of cortisone-induced cleft palate in the mouse have been examined. The SW/Fr strain, in which 6% of newborns have a cleft palate in the absence of treatment, has the greatest reactivity to cortisone of any strain tested so far and closes it palate comparatively late in development. After cortisone treatment, the mean of the distribution on palate closure stage is shifted towards later gestational ages without changing the variance. / The genetic basis for the DBA/2-C57BL/6 difference in susceptibility to cortisone-induced cleft palate is relatively simple. One dominant gene on chromosome 5 contributes predominantly to the strain difference in susceptibility, but the embryonic response appears also to be influenced by genes on the X chromosome. The H-2 haplotype does not affect the cortisone-induced cleft palate response in the two congenic strains C57BL/10 (B10) and B10.A by altering the stage of palate closure.

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