Marching to another clock

For several decades, researchers have studied the molecular mechanisms underlying circadian rhythms, the daily oscillations ubiquitous in biology. This basic clockwork is well understood in animal cells: Conserved clock proteins form a transcription-translation feedback loop that drives circadian oscillations of gene expression and downstream processes. These cellular clocks in peripheral tissues are hierarchically synchronized by a “master clock” in the brain [the suprachiasmatic nucleus (SCN) in mammals] responding to daylight, and also by other physiological signals such as feeding. On page 800 of this issue, Ray et al. (1) demonstrate that many circadian oscillations—in transcription, translation, and protein phosphorylation—can continue in mouse cells in the absence of an essential circadian clock gene, Bmal1 (brain and muscle ARNT-like 1). Thus, there might be other unknown clocks that also control circadian gene expression