在tRNA转位过程中,核糖体上延长因子G的形状变化
Jinzhong Lin1, Matthieu G Gagnon2, David Bulkley3
1Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT 06520-8114, USA.
Cell
|January 17, 2015
概括
延长因子G (EF-G) 在核糖体上移动tRNA和mRNA. 新的结构揭示了紧和延长状态之间的EF-G过渡,解释了tRNA转位,这是一种dityromycin可以阻止的过程.
科学领域:
- 分子生物学分子生物学
- 结构生物学 结构生物学
- 生物化学 生物化学
背景情况:
- 延长因子G (EF-G) 对于蛋白质合成至关重要,它催化了tRNA和mRNA在核糖体上的转位.
- 之前的结构研究主要显示EF-G在与核糖体结合的单一形状中.
研究的目的:
- 为了阐明EF-G在核糖体转位过程中的结构动态.
- 捕捉和描述以前未被观察到的EF-G状态在核糖体上.
主要方法:
- 原子分辨率晶体结构确定EF-G与编程核糖体结合.
- 分析EF-G在转位前,转位后和二铁胺被困状态中的分析.
主要成果:
- 获得了四个不同的EF-G-核糖体复合体的原子分辨率晶体结构.
- 观察到EF-G在转移前状态中的新型构造,也被dity.romycin捕获.
- 从紧到延长的EF-G形状的结构过渡促进了tRNA转位.
结论:
- EF-G样本在核糖体上比以前知道的更广泛的构造空间.
- 紧和延长的EF-G形状之间的过渡是tRNA转位的关键.
- 抗生素迪蒂罗米辛通过阻止这种必要的结构过渡来抑制转位.
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