tiK(+) toK(+): an embryonic clock?

During embryogenesis cells make appropriately timed developmental decisions . Both 'hourglass-like' and 'clock-like' mechanisms have been demonstrated to act as timers in early development. The cell cycle rhythm, using feedbac k circuits to drive cells unidirectionally, through checkpoints, is an exam ple of a clock-like timer, but how it operates to time developmental events is unclear. In other cell types, cyclic oscillations in K+ channel activit y, which parallel cell cycle and circadian rhythms, may be part of the timi ng mechanism. Changes in K+ oscillations accompany key developmental transi tions and oncogenic transformation. Channel blockade interferes pharmacolog ically with cell cycle initiation or progression, whereas channel over-expr ession can be oncogenic. K+ channel activity also exists in early mouse ooc ytes through to at least the blastocyst stage, and it oscillates in phase w ith the developmental cell cycles, being high in M/G(1) and low in S/G(2). It resembles physiologically the activity of the K+ channels of the eag- or erg-like families. Reverse transcriptase-polymerase chain reaction of mous e oocytes has revealed the presence of transcripts encoding both EAG- and E RG-like proteins throughout preimplantation development. Channel activity c ontinues to oscillate with a cell cycle periodicity in embryos from which t he nucleus has been removed, or after inhibition by puromycin of the cyclin B-cyclin-dependent kinase 1 driven component of the chromosomal cycle. Cha nnel oscillatory activity thus appears to be able to function autonomously of the chromosomal cycle and may represent a distinct oscillatory timing ac tivity with possible developmental significance.