酵母酵母的伴侣Sse1,Hsp110,控制细胞命运在内分泌网膜应激过程中
Mainak Pratim Jha1, Vignesh Kumar2,3, Asmita Ghosh2,3
1Protein Homeostasis Laboratory, Department of Life Sciences, School of Natural Sciences, Shiv Nadar Institution of Eminence, Delhi-NCR, Gautam Buddha Nagar, Greater Noida, Uttar Pradesh 201314, India.
G3 (Bethesda, Md.)
|April 5, 2024
概括
酵母细胞质的伴侣Sse1调节了细胞内网膜 (ER) 的压力. 它的缺失通过增强ER-unfolded protein response (ER-UPR) 信号传递,促进细胞存活,从而赋予了突尼卡米辛耐药性.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 压力反应应激反应
背景情况:
- Sse1是一种酵母Hsp110分子伴侣,在蛋白质平衡中具有已知的作用.
- 它的功能包括核酸交换,蛋白质分解和与蛋白质合成的关联.
- 细胞内膜网膜未折叠蛋白反应 (ER-UPR) 对于管理ER压力至关重要.
研究的目的:
- 为了研究细胞质伴侣Sse1在酵母ER-UPR中的作用.
- 为了确定Sse1缺失对突尼卡米辛诱导的ER压力的细胞反应的影响.
- 阐明Sse1在调节细胞分裂停止和在ER压力下生存能力方面的功能.
主要方法:
- 在SSE1,IRE1和HAC1.1之间进行遗传相互作用研究.
- 在突尼卡米辛压力下对酵母菌株 (sse1Δ和野生型) 的分析.
- 评估从多细胞体到单细胞体的核糖体重组.
- 评估ER-UPR激活,细胞分裂停止和细胞活力.
主要成果:
- SSE1 基因与 ER-UPR 传感器 IRE1 和 HAC1.1 发生相互作用.
- 缺少Sse1 (sse1Δ) 会导致依赖Ire1-Hac1信号的尼卡米辛耐药性.
- sse1Δ细胞表现出低效的核糖体重组,但更快的ER-UPR逆转和平衡恢复.
- 这种sse1Δ菌株逃脱了尼卡米辛诱导的细胞分裂停止,并显示出增加的活力.
结论:
- 细胞质伴侣Sse1是酵母ER应激反应的关键调节器.
- Sse1 影响 ER 蛋白质稳态和 ER-UPR 信号传递.
- Sse1控制压力诱导的细胞分裂停止和细胞死亡在尼卡米辛诱导的ER压力期间,影响酵母健康.
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