CELL-CYCLE CONTROL OF A LARGE-CONDUCTANCE K-CHANNEL IN MOUSE EARLY EMBRYOS()

THERE have been few investigations into the role of ion channels in ma mmalian early embryonic development1-4, despite studies showing that c hanges in ion channel activity accompany the early embryonic developme nt of non-mammalian species5-7 and the proliferation of mammalian cell s8-12. Here we report that a large-conductance, voltage-activated K+ c hannel is active in unfertilized mouse oocytes but is rarely observed in later embryos. The channel activity is linked to the cell cycle, be ing active throughout M and G1 phases, and switching off during the G1 -to-S transition. These changes in channel activity are accompanied by corresponding shifts in membrane potential. Inactivation of the chann el during S/G2 can be prevented by exposing the oocytes to dibutyryl c yclic AMP or forskolin, an activator of adenylyl cyclase. Inhibition o f protein synthesis with puromycin did not prevent inactivation of the channel at the end of G1 or its subsequent reactivation at the end of G2, indicating that the channel activity is not regulated by mitosis- promoting factor or cyclins.