Clock-dependent regulation of a homeostatic sleep center maintains daytime sleep and evening activity

Jun 28, 2025Current biology : CB

Internal clock controls a sleep-regulating brain area to keep daytime sleep and evening activity

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Abstract

Calcium levels in the dorsal fan-shaped body (dFSB) display a circadian rhythm, peaking during the daytime siesta.

23E10+ neurons in the dFSB promote sleep in a time-of-day-dependent manner, particularly influencing daytime sleep.
The role of these neurons in maintaining the daytime siesta is at least partially dependent on the period gene.
In vivo imaging reveals a circadian rhythm in calcium levels within the dFSB, aligning with the timing of the daytime siesta.
Loss of pigment dispersing factor (PDF) signaling leads to earlier downregulation of calcium activity, correlating with an earlier onset of night sleep in mutants.
Silencing the dFSB can restore the normal timing of night sleep onset in mutants lacking PDF signaling.

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Homeostatic sleep centers promote sleep in response to prolonged wakefulness, but their contribution to circadian-regulated daily sleep is still unclear. Do neuronal circuits driving rebound sleep after extended wakefulness also drive circadian-gated sleep, or does rebound sleep differ on a neurophysiological level from daily baseline sleep? We observed in Drosophila that 23E10+ neurons, which include a homeostatic sleep center, the dorsal fan-shaped body (dFSB),promote sleep in a time-of-day-dependent manner-the neurons play the strongest role in the maintenance of daytime sleep, and this effect on the siesta maps to cholinergic neurons within the dFSB. We asked whether 23E10+ neurons interact with the circadian clock to regulate daily sleep and find their role in maintaining the daytime siesta is at least partially dependent on the period gene. Through in vivo imaging, we show that calcium levels in the dFSB display a circadian rhythm, with a peak coinciding with the daytime siesta. In the absence of a period, the 24-h rhythm is lost, but a daytime increase in calcium activity is maintained. Loss of pigment dispersing factor (PDF) signaling causes premature downregulation of calcium activity in the dFSB, coinciding with the earlier truncation of the siesta in pdfr mutants and resulting in an earlier onset of night sleep. Silencing the dFSB is sufficient to rescue the timing of night sleep onset in pdfr mutants. These results indicate that the dFSB, a homeostatic sleep center, relies on the circadian clock to restrict sleep drive to specific times of day. 1, 2, 3, 4, 5

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Clock-dependent regulation of a homeostatic sleep center maintains daytime sleep and evening activity

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