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SIK3–HDAC4 in the suprachiasmatic nucleus regulates the timing of arousal at the dark onset and circadian period in mice
SIK3-HDAC4 in the brain’s internal clock controls waking time at nightfall and daily rhythm length in mice
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Abstract
Salt-inducible kinase 3 (SIK3) deficiency in specific neurons lengthened the behavioral circadian cycle in laboratory mice.
- Deficiency of SIK3 in GABAergic or neuromedin S-producing neurons delayed the peak of arousal without affecting daily sleep amounts.
- A gain-of-function mutation in GABAergic neurons resulted in earlier activity onset and a shorter .
- Loss of SIK3 in arginine vasopressin-producing neurons also lengthened the circadian cycle, but did not change the timing of arousal.
- Heterozygous deficiency of histone deacetylase 4 (HDAC4) shortened the circadian cycle, while a mutant resistant to SIK3 phosphorylation delayed arousal timing.
- Phase-delayed expressions of core clock genes were observed in the liver of mice lacking SIK3 in GABAergic neurons.
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Key numbers
15.1 ± 0.6 h
Delayed
timing for SIK3-deficient GABAergic neurons.
23.4 ± 0.0 h
Length
for mice with induced gain-of-function allele in GABAergic neurons.
ZT14.0 ± 0.6
Timing
timing for NMS-positive neuron SIK3-deficient mice.