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Although sleep is one of the most conserved behaviors, the intracellular mechanism regulating sleep/wakefulness remains unknown. We recently identified a protein kinase, SIK3, as a sleep-regulating molecule. Mice that lack a well-conserved protein kinase A (PKA) phosphorylation site, S551, showed longer non-rapid eye movement (NREM) sleep and increased NREMS delta density. S551 of SIK3 is conserved in other members of the SIK family, such as SIK1 (S577) and SIK2 (S587). Here, we examined whether the PKA phosphorylation sites of SIK1 and SIK2 are involved in sleep regulation by generating  Sik1   S577A   and  Sik2   S587A   mice. The homozygous  Sik1   S577A   mice showed a shorter wake time, longer NREMS time, and higher NREMS delta density than the wild-type mice. The heterozygous and homozygous  Sik2   S587A   mice showed increased NREMS delta density. Both the  Sik1   S577A   and  Sik2   S587A   mice exhibited proper homeostatic regulation of sleep need after sleep deprivation. Despite abundant expression of  Sik1  in the suprachiasmatic nucleus, the  Sik1   S577A   mice showed normal circadian behavior. Although  Sik2  is highly expressed in brown adipose tissue, the male and female  Sik2   S587A   mice that were fed either a chow or high-fat diet showed similar weight gain as the wild-type littermates. These results suggest that PKA-SIK signaling is involved in the regulation of sleep need.

Loss of the conserved PKA sites of SIK1 and SIK2 increases sleep need