The bacterial translation stress response.

The bacterial translation stress response.
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DOI:
10.1111/1574-6976.12083
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发表时间:
2014-11
影响因子:
11.3
通讯作者:
Wilson DN
Wilson DN
中科院分区:
生物学1区
文献类型:
--
作者:
Starosta AL;Lassak J;Jung K;Wilson DN

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在它们的一生中,细菌需要感知和应对环境压力。因此,这种应激反应可能需要在转录和翻译水平上进行剧烈的细胞重编程。本文综述了与细菌翻译器相互作用以响应和科普不同类型的环境应激的蛋白质因子。例如,严格因子RelA与核糖体相互作用以在营养缺乏下产生ppGpp,而已经鉴定了多种因子在不利的生长条件下结合核糖体以关闭(RelE、pY、RMF、HPF和EttA)或重新编程(MazF、EF 4和BipA)翻译。已经鉴定了其他因素,这些因素可以挽救由于应激诱导的mRNA截短(tmRNA、ArfA、ArfB)、不利蛋白序列的翻译(EF-P)、热休克诱导的亚基解离(Hsp 15)或抗生素抑制(TetM、FusB)而停滞的核糖体。了解细菌细胞如何响应压力的机制不仅将为翻译调控提供基本的见解,而且也将是确定开发新型抗菌剂的新靶点的重要一步。
Throughout their life, bacteria need to sense and respond to environmental stress. Thus, such stress responses can require dramatic cellular reprogramming, both at the transcriptional as well as the translational level. This review focuses on the protein factors that interact with the bacterial translational apparatus in order to respond to and cope with different types of environmental stress. For example, the stringent factor RelA interacts with the ribosome to generate ppGpp under nutrient deprivation, whereas a variety of factors have been identified that bind to the ribosome under unfavorable growth conditions to shut-down (RelE, pY, RMF, HPF and EttA) or re-program (MazF, EF4 and BipA) translation. Additional factors have been identified that rescue ribosomes stalled due to stress-induced mRNA truncation (tmRNA, ArfA, ArfB), translation of unfavorable protein sequences (EF-P), heat shock induced subunit dissociation (Hsp15) or antibiotic inhibition (TetM, FusB). Understanding the mechanism of how the bacterial cell responds to stress will not only provide fundamental insight into translation regulation, but will also be an important step to identifying new targets for the development of novel antimicrobial agents.
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