A salt-induced kinase is required for the metabolic regulation of sleep.,PLOS Biology

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A salt-induced kinase is required for the metabolic regulation of sleep.
PLOS Biology ( IF 7.8 ) Pub Date : 2020-04-21 , DOI: 10.1371/journal.pbio.3000220
Jeremy J Grubbs _{1,

2} , Lindsey E Lopes ₂ , Alexander M van der Linden ₁ , David M Raizen ₂

Affiliation

Many lines of evidence point to links between sleep regulation and energy homeostasis, but mechanisms underlying these connections are unknown. During Caenorhabditis elegans sleep, energetic stores are allocated to nonneural tasks with a resultant drop in the overall fat stores and energy charge. Mutants lacking KIN-29, the C. elegans homolog of a mammalian Salt-Inducible Kinase (SIK) that signals sleep pressure, have low ATP levels despite high-fat stores, indicating a defective response to cellular energy deficits. Liberating energy stores corrects adiposity and sleep defects of kin-29 mutants. kin-29 sleep and energy homeostasis roles map to a set of sensory neurons that act upstream of fat regulation as well as of central sleep-controlling neurons, suggesting hierarchical somatic/neural interactions regulating sleep and energy homeostasis. Genetic interaction between kin-29 and the histone deacetylase hda-4 coupled with subcellular localization studies indicate that KIN-29 acts in the nucleus to regulate sleep. We propose that KIN-29/SIK acts in nuclei of sensory neuroendocrine cells to transduce low cellular energy charge into the mobilization of energy stores, which in turn promotes sleep.

中文翻译：

睡眠的代谢调节需要盐诱导激酶。

许多证据表明睡眠调节和能量稳态之间存在联系，但这些联系背后的机制尚不清楚。在秀丽隐杆线虫睡眠期间，能量储存被分配给非神经任务，从而导致整体脂肪储存和能量消耗下降。缺乏KIN-29（一种哺乳动物盐诱导激酶（SIK）的线虫同源物，可发出睡眠压力信号）的突变体尽管脂肪储存量高，但ATP水平较低，这表明对细胞能量缺乏的反应有缺陷。释放能量储存可纠正 kin-29 突变体的肥胖和睡眠缺陷。 kin-29睡眠和能量稳态作用映射到一组感觉神经元，这些神经元作用于脂肪调节以及中枢睡眠控制神经元的上游，表明调节睡眠和能量稳态的分层体细胞/神经相互作用。 kin-29 和组蛋白脱乙酰酶 hda-4 之间的遗传相互作用以及亚细胞定位研究表明，KIN-29 在细胞核中发挥调节睡眠的作用。我们提出 KIN-29/SIK 在感觉神经内分泌细胞的细胞核中起作用，将低细胞能量电荷转导为能量储存的动员，从而促进睡眠。

更新日期：2020-04-21

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