冬眠因素RMF,HPF和YfiA如何关闭蛋白质合成
Yury S Polikanov1, Gregor M Blaha, Thomas A Steitz
1Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT 06520-8114, USA.
Science (New York, N.Y.)
|May 19, 2012
概括
细菌通过非激活核糖体,在静止阶段停止蛋白质的产生. 这项研究揭示了核糖体调节因子 (RMF) 和冬眠促进因子 (HPF) 如何促进100S二极体的形成,而YfiA则形成非活性70S单体.
科学领域:
- 细菌生理学 细菌生理学
- 结构生物学 结构生物学
- 分子生物学分子生物学
背景情况:
- 欧细菌通过将核糖体无活化成100S二聚体或70S单聚体过渡到静止阶段.
- 大肠杆菌中的核糖体不活化涉及核糖体调节因子 (RMF),冬眠促进因子 (HPF) 或YfiA蛋白.
- 了解这些机制对于细菌的生存和应激反应至关重要.
研究的目的:
- 阐明 Eubacteria 中通过静止相因子对核糖体无活化的结构基础.
- 确定与RMF,HPF和YfiA复合的Thermus thermophilus 70S核糖体的高分辨率晶体结构.
- 调查这些因素如何阻止翻译并促进核糖体二分化.
主要方法:
- 高分辨率的晶体学.
- 对Thermus thermophilus 70S核糖体复合物的结构分析
- 结合部位的比较分析.
主要成果:
- 在70S核糖体上的RMF的结合部位与mRNAShine-Dalgarno序列重叠,抑制mRNA-rRNA相互作用.
- HPF和YfiA与涉及mRNA,tRNA和启动因子的重叠部位结合,防止翻译启动.
- 结合RMF和HPF会诱导30S头域的形状变化,促进100S二聚体的形成,这种机制在YfiA中没有观察到.
结论:
- RMF和HPF通过不同的结构相互作用和构造变化促进100S核糖体二分化.
- YfiA通过防止翻译启动而未诱导二分化,使核糖体作为70S单体失活.
- 这些发现提供了关键的结构洞察力细菌核糖体调节在静止阶段.
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