细胞机制连接了细胞内质网膜遗传和细胞周期调节的核基因组
bioRxiv : the preprint server for biology
|September 15, 2025
概括
细胞内膜网膜 (ER) 的压力通过影响Bud2和Shs1蛋白质来破坏细胞分裂. 这项研究揭示了ER完整性如何影响细胞周期进展和线粒体忠实性.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 细胞内膜网膜 (ER) 的压力激活了ER监测 (ERSU) 途径,阻止了细胞分裂.
- 在ER完整性和细胞循环调节之间的分子联系仍然不清楚.
研究的目的:
- 阐明连接ER稳态与细胞周期控制的分子机制.
- 调查Bud2和Shs1在ER监控通路中的作用.
主要方法:
- 在酵母模型中研究了ER应激对Bud2局部化和功能的影响.
- 使用了酵母基因,包括shs1-ΔCTD突变和Bud2过度表达.
- 与细胞极性,动力学和基因组分离相关的观察到的表型.
主要成果:
- ER应力分散Bud2,一个细胞极性调节器,导致螺旋误导和基因组分离错误.
- 一个截断的Shs1蛋白 (shs1-ΔCTD) 模仿了ER压力诱导的Bud2分散和延迟细胞周期重新进入.
- 在shs1-ΔCTD突变体中,Bud2过度表达挽救了生长缺陷.
结论:
- 通过选择性调节Bud2和Shs1.1,ER完整性会影响细胞周期的进展.
- 这一途径作为ER状态和线粒体忠实性之间的直接联系.
- 研究结果揭示了一种协调有机体遗传,细胞骨和核分裂的新机制.
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