K(ATP) channel activity is required for hatching in Xenopus embryos.

Abstract

A growing body of work suggests that the activity of ion channels and pumps is an important regulatory factor in embryonic development. We are beginning to identify functional roles for proteins suggested by a survey of expression of ion channel and pump genes in Xenopus and chick embryos (Rutenberg et al. [2002] Dev Dyn 225, this issue). Here, we report that the ATP-sensitive K(+) channel protein is present in the hatching gland of Xenopus embryos; moreover, we show that its activity is necessary for hatching in Xenopus. Pharmacologic inhibition of K(ATP) channels not only specifically prevents the hatching process but also greatly reduces the endogenous expression of Connexin-30 in the hatching gland. Based on recent work which showed that gap-junctional communication mediated by Cx30 in the hatching gland was required for secretion of the hatching enzyme, we propose that K(ATP) channel activity is upstream of Cx30 expression and represents a necessary endogenous step in the hatching of the Xenopus embryo.