A phosphorylation-deficient mutant of , a homolog of , alters circadian sleep regulation by PDF neurons in .

Sleep behavior has been observed from non-vertebrates to humans. mutation in mice resulted in a notable increase in sleep and was identified as an exon-skipping mutation of the gene, conserved among animals. The skipped exon includes a serine residue that is phosphorylated by protein kinase A. Overexpression of a mutant gene with the conversion of this serine into alanine () increased sleep in both mice and the fruit fly . However, the mechanism by which increases sleep remains unclear. Here, we found that overexpression in all neurons increased sleep under both light-dark (LD) conditions and constant dark (DD) conditions in . Additionally, overexpression of only in PDF neurons, which are a cluster of clock neurons regulating the circadian rhythm, increased sleep during subjective daytime while decreasing the amplitude of circadian rhythm. Furthermore, suppressing overexpression specifically in PDF neurons in flies overexpressing in all neurons reversed the sleep increase during subjective daytime. These results indicate that alters the circadian function of PDF neurons and leads to an increase in sleep during subjective daytime under constant dark conditions.