睡眠(系统调用)
磷酸化
苏氨酸
生物
突变体
激酶
睡眠剥夺
神经科学
细胞生物学
生物化学
昼夜节律
丝氨酸
基因
计算机科学
操作系统
作者
Yang Li,Chengang Li,Yuxiang Liu,Jiabin Yu,Jingqun Yang,Yunfeng Cui,Tao V Wang,Chaoyi Li,Lifen Jiang,Mengmeng Song,Yi Rao
出处
期刊:Genetics
[Oxford University Press]
日期:2023-07-21
卷期号:225 (1)
标识
DOI:10.1093/genetics/iyad136
摘要
Abstract Sleep need drives sleep and plays a key role in homeostatic regulation of sleep. So far sleep need can only be inferred by animal behaviors and indicated by electroencephalography (EEG). Here we report that phosphorylation of threonine (T) 221 of the salt-inducible kinase 3 (SIK3) increased the catalytic activity and stability of SIK3. T221 phosphorylation in the mouse brain indicates sleep need: more sleep resulting in less phosphorylation and less sleep more phosphorylation during daily sleep/wake cycle and after sleep deprivation (SD). Sleep need was reduced in SIK3 loss of function (LOF) mutants and by T221 mutation to alanine (T221A). Rebound after SD was also decreased in SIK3 LOF and T221A mutant mice. By contrast, SIK1 and SIK2 do not satisfy criteria to be both an indicator and a controller of sleep need. Our results reveal SIK3-T221 phosphorylation as a chemical modification which indicates and controls sleep need.
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