在葡萄糖饥饿期间,TOR无活化触发了rDNA中的异染色素的形成
Hayato Hirai1, Yuki Sen2, Miki Tamura1
1Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Komaba 3-8-1, Meguro-ku, Tokyo 153-8902, Japan.
Cell reports
|November 1, 2023
概括
分裂酵母通过基因组修饰和在营养饥饿时形成异染色素来抑制核糖体基因,与芽酵母不同. 这种机制涉及TORC1解离和H3K9甲基化,可能在哺乳动物中保存.
科学领域:
- 分子生物学分子生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 酵母遗传学 酵母遗传学
背景情况:
- 环境暗示,如营养缺乏,通过基因素修饰引发基因表达调节.
- 营养物质的枯竭使拉帕素 (TOR) 途径的目标不活化,从而减少了芽发酵酵母中的核糖体基因表达.
- 不同种类的生物体中这些调节机制的保护尚未得到充分理解.
研究的目的:
- 为了研究裂变酵母Schizosaccharomyces pombe中的核糖体基因转录抑制机制.
- 为了比较裂变酵母和芽酵母Saccharomyces cerevisiae之间的调节机制.
- 探索哺乳动物中这些机制的潜在保护.
主要方法:
- 在饥饿时对rDNA区域的TORC1局部化和解离的分析.
- 评估基因素H3氨酸9 (H3K9) 甲基化和异色染色体的形成.
- 对转录因子Atf1和基因素伴奏子FACT的作用的评估.
主要成果:
- 与发芽酵母相比,裂变酵母通过不同的机制抑制核糖体基因转录.
- 在饥饿时,TORC1与rDNA区域分离,导致H3K9甲基化和异染色素的增加.
- Atf1的解离和FACT的积累促进了这种异染色素的形成.
结论:
- 裂变酵母采用一种独特的表观遗传机制,涉及TORC1,H3K9甲基化和异染色素的形成,用于核糖体基因抑制.
- 这种机制与在芽酵母中观察到的TOR通路无活化有显著差异.
- 已识别的机制可能在哺乳动物中保留,特别是那些拥有Suv39H1和HP1.1的哺乳动物.
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