TOR信号通路控制着营养调节转录因子的核定位
Nature
|December 22, 1999
概括
酵母中的TOR信号通路通过在细胞质中保持关键的转录因子来控制营养代谢. 这种机制阻止了与饥饿和碳源调节相关的基因的表达.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 拉帕amycin (TOR) 信号通路的目标调节细胞生长,以应对Saccharomyces cerevisiae中的和碳等营养素.
- 托尔激酶 (TOR1和TOR2) 通过TAP42管理蛋白质合成和降解,但它们在核事件中的作用,特别是抑制饥饿诱导的转录,仍然不清楚.
研究的目的:
- 阐明TOR信号通路控制核事件的机制,特别是对饥饿特异性转录的抑制.
- 研究TOR信号如何影响由和碳可用性调节的基因表达.
主要方法:
- 研究了由TOR-依赖酸化介导的GLN3和URE2之间的相互作用.
- 分析了TAP42和酸酶SIT4在GLN3酸化和细胞质保留中的作用.
- 研究了MSN2和MSN4与BMH2的结合,这是一个依赖TOR的过程.
主要成果:
- 托尔信号促进了GATA转录因子GLN3与URE2的关联,需要托尔依赖的GLN3酸化.
- GLN3酸化和细胞质局部化依赖于TOR效应器TAP42,并与酸酶SIT4相对抗.
- 通过增强转录激活剂MSN2和MSN4与细胞质蛋白BMH2的结合,TOR信号抑制碳源调节的基因.
结论:
- TOR信号通路通过将多个转录因子 (包括GLN3,MSN2和MSN4) 隔离在细胞质中,广泛调节营养代谢.
- 这种TOR的细胞质封存阻止了与营养限制和特定碳来源相关的基因的转录.
相关概念视频
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