Scholarlink

<p>Prolonged sleep deprivation (Pr-SD) causes death in many species. While various mechanisms related to sleep regulation or this fatal consequence of sleep loss have been identified, the core molecular basis linking Pr-SD-induced lethality and sleep homeostasis remains unknown in mammals. A critical “point of no return (PONE)” status in Pr-SD subjects is highlighted in classic research, and characterizing PONE status could help uncover this mystery. Using a Pr-SD model and a reliable PONE status prediction method, we show that mice in PONE exhibit an inability to enter natural sleep, and significant disruptions in brain phosphoproteome, independent of deprivation time but closely linked to PONE status. Brain kinase or phosphatase dysfunction influences PONE status development and leads to corresponding sleep aberration concurrently. Daily 80-min recovery sleep significantly delays PONE onset and restores brain phosphoproteome. The harmful effects of excessive kinase activity on PONE development can be eliminated by combining recovery sleep and compensatory phosphatase expression. We conclude that sleep is crucial for maintaining brain phosphoproteome homeostasis, whose disruption may impact both Pr-SD-induced lethality and sleep regulation.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Sleep prevents brain phosphoproteome disruption to safeguard survival

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年6月24日

查看全文
  • Jing Ma,
  • Juhang Liu,
  • Yu Li,
  • Yikui Zhao,
  • Yu Tian,
  • Bing Hu,
  • Kaiyue Yan,
  • Ying Li,
  • Kaihang Ding,
  • Xiangyu Wang,
  • Huiwen Tian,
  • Wen Si,
  • Ketong Liu,
  • Huiran Zhang,
  • Chongchong Zhao,
  • Guangfu Wang,
  • Zhiqiang Wang

摘要

Prolonged sleep deprivation (Pr-SD) causes death in many species. While various mechanisms related to sleep regulation or this fatal consequence of sleep loss have been identified, the core molecular basis linking Pr-SD-induced lethality and sleep homeostasis remains unknown in mammals. A critical “point of no return (PONE)” status in Pr-SD subjects is highlighted in classic research, and characterizing PONE status could help uncover this mystery. Using a Pr-SD model and a reliable PONE status prediction method, we show that mice in PONE exhibit an inability to enter natural sleep, and significant disruptions in brain phosphoproteome, independent of deprivation time but closely linked to PONE status. Brain kinase or phosphatase dysfunction influences PONE status development and leads to corresponding sleep aberration concurrently. Daily 80-min recovery sleep significantly delays PONE onset and restores brain phosphoproteome. The harmful effects of excessive kinase activity on PONE development can be eliminated by combining recovery sleep and compensatory phosphatase expression. We conclude that sleep is crucial for maintaining brain phosphoproteome homeostasis, whose disruption may impact both Pr-SD-induced lethality and sleep regulation.