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The bacterial translation stress response

机译:细菌翻译应激反应

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摘要

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.
机译:在细菌的整个生命中,它们都需要感知并应对环境压力。因此,这样的应激反应在转录和翻译水平上都可能需要剧烈的细胞重编程。这篇综述着重于与细菌翻译设备相互作用的蛋白质因子,以响应和应对不同类型的环境压力。例如,严格因子RelA在营养剥夺下与核糖体相互作用,生成ppGpp,而已发现在不利的生长条件下,与核糖体结合的多种因子会关闭(RelE,pY,RMF,HPF和EttA)或重新编程(MazF,EF4和BipA)翻译。已经确定了其他因素,即救援核糖体因压力诱导的mRNA截断(tmRNA,ArfA,ArfB),不利的蛋白质序列翻译(EF-P),热休克诱导的亚基解离(Hsp15)或抗生素抑制(TetM,FusB)而停滞)。了解细菌细胞如何应对压力的机制不仅将提供对翻译调控的基本了解,而且还将是确定开发新型抗菌剂的新靶标的重要步骤。

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