蛋白酶介导的PRC1解离促进了H2AK119ub在应激反应期间的重塑
Wei Cui1, Qingyang Li1,2, Jinsong Wei1
1MOE Key Laboratory of Biosystems Homeostasis & Protection, College of Animal Sciences, Zhejiang University, 310058, Hangzhou, China.
The EMBO journal
|March 12, 2026
概括
蛋白酶CAPN3在应激过程中从染色质中释放聚合体抑制复合体1 (PRC1). 这种表观遗传重塑降低了基因素H2AK119ub水平,促进了细胞应激反应.
科学领域:
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 分子生物学分子生物学
- 细胞应激反应的应激反应
背景情况:
- 染色体结构对于细胞对压力的反应至关重要.
- 聚合体抑制复合体1 (PRC1) 通过H2AK119ub.通过染色体进行紧.
- 从染色质中解离PRC1的机制尚未完全理解.
研究的目的:
- 为了研究蛋白酶在PRC1与染色质分离中的作用.
- 为了阐明细胞应激期间PRC1释放的机制.
主要方法:
- 诱导肝损伤和热冲击模型.
- 分析PRC1亚单元的裂变和解离.
- 对H2AK119ub水平的量化.
主要成果:
- 在压力时,Calpain 3 (CAPN3) 蛋白酶激活.
- 非核心PRC1子单元的CAPN3蛋白质分解.
- 压力诱导的CAPN3促进PRC1解离和H2AK119ub减少.
结论:
- 在应对压力时,CAPN3调解了PRC1与染色质的快速解离.
- 这揭示了蛋白酶驱动的染色质重塑的表观遗传机制.
- CAPN3 是压力诱导的表观遗传变化的关键调节者.
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