触发因子和DnaK合作折叠新合成的蛋白质
E Deuerling1, A Schulze-Specking, T Tomoyasu
1Institut für Biochemie und Molekularbiologie, Freiburg, Germany.
Nature
|August 24, 1999
概括
触发因子,一个与核糖体相关的伴侣,对于大肠杆菌中蛋白质折叠至关重要. 它与Hsp70 DnaK的合作防止了蛋白质聚合,并确保了细胞活力.
科学领域:
- 微生物学 微生物学
- 分子生物学分子生物学
- 蛋白质折叠 蛋白质的折叠
背景情况:
- 在新生的蛋白质折叠中分子陪伴者的作用尚未完全理解.
- 在大肠杆菌中,GroEL和Hsp70 DnaK对于在中等温度下折叠并非必不可少.
- 核糖体关联触发因子是新生多的主要伴侣.
研究的目的:
- 为了研究触发因子在蛋白质折叠中的体内功能.
- 确定触发因子和DnaK之间的功能关系.
- 阐明大肠杆菌中伴侣的合作机制.
主要方法:
- 基因删除突变 (delta tig::kan) 在大肠杆菌中被创造出来.
- 分析了组合突变 (delta tig::kan和delta dnaK) 的情况.
- 在各种条件下评估了蛋白质聚合和与DnaK的关联.
主要成果:
- 缺乏触发因子的大肠杆菌没有生长或折叠缺陷.
- 结合触发因子和DnaK缺乏导致合成致命性.
- 触发因子缺乏细胞中的DnaK枯竭导致了大量的细胞质蛋白聚合.
结论:
- 触发因子在体内表现出对一般蛋白质折叠的伴侣活性.
- 触发因子和DnaK合作,确保适当的蛋白质折叠和细胞活力.
- 在中等生长温度下,任何一个陪伴者对折叠和生存能力都不是个人必不可少的.
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