The NFκB is required for behavioral and molecular correlates of sleep homeostasis in .

The nuclear factor binding the κ light chain in B-cells (NFκB) is involved in a wide range of cellular processes including development, growth, innate immunity, and sleep. However, efforts have been limited toward understanding how specific NFκB transcription factors function in sleep. fruit flies carry three genes encoding NFκB transcription factors, , (), and . We previously found that loss of the gene from fat body suppressed daily nighttime sleep, and abolished infection-induced sleep. Here we show that regulates daily sleep and recovery sleep following prolonged wakefulness. Mutants of showed reduced daily sleep and suppressed recovery in response to sleep deprivation. Pan-neuronal knockdown of strongly suppressed daily sleep, indicating that in contrast to , functions from the central nervous system to regulate sleep. Based on the distribution of a -associated GAL4 driver, we hypothesized that its effects on sleep were mediated by the pars intercerebralis (PI). While RNAi knock-down of in the PI reduced daily sleep, it had no effect on the recovery response to sleep deprivation. However, recovery sleep was suppressed when RNAi knock-down of was distributed across a wider range of neurons. Induction of the () antimicrobial peptide by sleep deprivation was suppressed in mutants and pan-neuronal over-expression of also suppressed the mutant phenotype. Together, these findings indicate that functions from brain to target and to promote sleep.