Maternal treatment with cortisone accelerates eyelid closure and other developmental fusion processes in fetal mice

Cortisone acetate administered to pregnant CBA/J and SWV/Bc mice at 30 to 100 mg kg-1 on day 14 of gestation causes accelerated development of eyelid closure, digit fusion and fusion of pinnae to the scalp on day 16 of gestation. Eyelid closure seems to be accelerated more than hindlimb digit fusion. The results support the hypothesis that the prevention of the open-eye birth defect in lgMl/lgMl mutant mice by cortisone is through a shift of eye closure to an earlier chronological or morphological stage, and that the lgMl mutation causes delay in eyelid development and closure. Most previous studies of the effects of glucocorticoids on morphological development have focussed on high doses that induce defects, such as cleft palate, and on treatment earlier in gestation. In the studies reported here, lower doses were used and an acceleration of apparently normal development was observed. The results support the possibility that the gene regulatory effects of physiological levels of glucocorticoids are involved in normal morphological development of mammalian fetuses. The regulation of genes is far less well understood for morphological development than for biochemical differentiation. The responses of the four morphological traits described in this paper seem to offer a route to some greater insight into the genetic regulation of morphology.