More Rhythm and Blues
A few weeks back I mused about recent research showing that disruption of normal circadian rhythms can lead to all manner of health disorders. The work was intriguing because most of us take long flights to different time zones, work all night to meet a deadline, or otherwise perturb our normal rhythms. Left unsolved, however, is the problem of how to explain the results at the biochemical level.
Now comes a collaboration between researchers at Penn and Harvard that pinpoints at least one chemical change that may be a culprit in mediating the ill effects of circadian rhythm gone bad (Science 333: 6022 [March 11, 2011], 1315–1319). The perpetrator is histone deacetylase 3 (HDAC3), an enzyme that removes acetyl groups from lysine amino acids present in histones. The results show that there are about 14,000 specific acetylations at histone DNA binding sites present when experimental mice are sleepy and inactive, but only about 100 when the critters are actively scurrying about, eating, and doing normal mousy activities.
Mice aren’t human, of course, and they reverse our customary pattern by being active at night and asleep during the day. Still, acetylation of histones is a key regulator of gene expression, so the huge diurnal variation seen in these experiments offers a clear lead to where the biological clock resides that controls circadian rhythm.
Alas, no cure yet for jet lag, but these results bring us one step closer to relieving that particularly vexing aspect of contemporary travel.