Circadian clocks are regulated with the precision of a Swiss watch. They continue to tick without external cues, but they can also be reset (or 'entrained') by environmental signals such as light–dark cycles. But how? In December's Nature Neuroscience, Paolo Sassone-Corsi, David Allis and colleagues link light entrainment to the dynamic remodelling of chromatin.

In mammals, the nerve centre of the circadian clock is the hypothalamic suprachiasmatic nucleus (SCN). Animals kept in darkness and given a pulse of light during the 'subjective night' (the time of day corresponding to the dark period in a normal light–dark cycle) show a phase-shifting of normal rhythms, accompanied by the expression of various clock and immediate-early genes in the SCN. These changes in gene expression are thought to be responsible for the light entrainment.

What controls the dynamic regulation of these genes at the chromosomal level? To investigate, Sassone-Corsi and colleagues studied the effects of a night-time light pulse on phosphorylation of histone H3 — a central event in the remodelling of chromatin. They observed such light-induced phosphorylation in the SCN of mice, but not in other structures tested (the retina and pineal gland).

The authors next showed that a time course of H3 phosphorylation parallels the induction profile of an early-response gene — c-fos — in the same SCN neurons, indicating that the two events are linked. Moreover, when mice were given baclofen, a drug that inhibits light-induced phase-shifts during the subjective night, both phosphorylation of histone H3 and expression of c-fos were reduced. Again, the implication is that one signalling pathway controls both events.

These results may indicate, conclude the authors, that “dynamic chromatin remodelling in the SCN occurs in response to a physiological stimulus in vivo”. And the next step in unravelling this complex molecular clockwork will be to identify the light-induced kinase that is responsible.