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.