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RNA质量控制因子核化Clr4/SUV39H并触发构成性的异染色体组合

Jasbeer S Khanduja¹, Richard I Joh¹, Monica M Perez¹

¹Massachusetts General Hospital Krantz Family Center for Cancer Research and Department of Medicine, Harvard Medical School, Charlestown, MA 02129, USA.

|May 30, 2024

概括

长非编码RNAs (lncRNAs) 和RNA质量控制因子启动异染色体的形成. 这种独立于小RNA的过程,通过RNA干扰来强化基底状态以实现强大的表观遗传沉默.

科学领域:

表观遗传学和基因调控
分子生物学
染色体生物学

背景情况:

细胞的异性染色体形成依赖于素H3 lysine 9三甲基化 (H3K9me),主要由Suv39家族蛋白质介导.
目前的裂变酵母模型表明,与Argonaute1相关的小RNAs (sRNAs) 在H3K9me的中间体中核化Clr4/SUV39H.
在异色素蛋白中Suv39蛋白的精确核化机制尚不完全理解.

研究的目的:

在没有sRNA和H3K9me的情况下研究H3K9甲基转移酶Clr4/SUV39H的核化机制.
阐明长非编码RNAs (lncRNAs) 和RNA质量控制因子在启动异染色体形成中的作用.
了解脱和甲基化在H3K9me传播中的相互作用.

主要方法:

在裂变酵母中进行基因分析,以研究sRNA缺乏和H3K9me缺乏条件下的异染色体形成.
对MTREC/PAXT复合物与lncRNAs和Clr4/SUV39H的相互作用进行生物化学测试.
基因组修饰 (H3K9me和H3K9乙化) 的分析,以追踪异染色体的建立和扩散.

主要成果:

Mtl1和Red1核心 (MTREC) /PAXT复合体以sRNA独立的方式在异色IncRNA中核化Clr4/SUV39H.
通过不同的机制,Sir2和Clr3基因组脱乙酶在IncRNA核化部位积聚.
H3K9脱乙和甲基化的代循环促进了Clr4/SUV39H的传播,建立了H3K9me的基础状态.
该RNA干扰 (RNAi) 机制在中粒体上放大H3K9me信号,增加异色素的建立.

结论:

lncRNAs和RNA质量控制因子作为异染色体的关键核化中心.
一个涉及lncRNAs的sRNA独立途径建立了H3K9me的基础水平.
这项研究揭示了表观遗传沉默的新机制,突出了lncRNAs和RNA质量控制在异色素蛋白形成中的双重作用.

关键词:

其他:标签: 美国美国脱乙和甲基化 H3K9 MTREC/NURS 进行测试美国您的意思是新增异色素的形成异色素核化长非编码RNA 核外体

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