通过HflXr进行替代性核糖体循环的机制性见解
Savannah M Seely1, Ritwika S Basu2, Matthieu G Gagnon1,2,3,4
1Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Nucleic acids research
|February 26, 2024
概括
细菌使用HflXr救援因子在压力时分离停滞的核糖体. 这项研究揭示了HflXrr.
科学领域:
- 分子生物学分子生物学
- 微生物学 微生物学
- 结构生物学 结构生物学
背景情况:
- 在细胞压力 (热冲击,抗生素) 期间,核糖体在mRNA上停滞不前,停止蛋白质合成.
- 细菌使用核糖体救援因子来重新启动蛋白质合成.
- HflXr是HflX的同源,HflX是一种参与核糖体循环的GTPase.
研究的目的:
- 为了阐明由Listeria monocytogenes HflXr.的核糖体循环的机制.
- 要了解HflXr解离器是如何阻碍70S核糖体的.
主要方法:
- 时间分辨率冷电子显微镜 (cryo-EM).
- 对HflXr与70S核糖体结合的结构分析.
主要成果:
- 在50S核糖体子单元上,HflXr取代了H69螺旋.
- HflXr在30S子单元的平台域中引发了显著的重排.
- 这些结构变化破坏了多个子单位间的桥梁 (B2b,B2c,B4,B7a,B7b).
结论:
- HflXr采用一种独特的核糖体循环机制,与RRF和EF-G不同.
- 这种机制需要对核糖体进行广泛的结构重塑.
- 与HflX的相似性表明,这种替代的核糖体救援途径在 prokaryotes 中广泛存在.
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