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移动遗传元件对 LexA 的利用和滥用。

The Use and Abuse of LexA by Mobile Genetic Elements.

机构信息

Department of Biological and Environmental Science and Nanoscience Center, University of Jyvaskyla, PO Box 35, F-40014 Jyvaskyla, Finland.

Institute of Microbiology and Infection, School of Biosciences, University of Birmingham, Birmingham, B15 2TT, UK.

出版信息

Trends Microbiol. 2016 May;24(5):391-401. doi: 10.1016/j.tim.2016.02.009. Epub 2016 Mar 9.

DOI:10.1016/j.tim.2016.02.009
PMID:26970840
Abstract

The SOS response is an essential process for responding to DNA damage in bacteria. The expression of SOS genes is under the control of LexA, a global transcription factor that undergoes self-cleavage during stress to allow the expression of DNA repair functions and delay cell division until the damage is rectified. LexA also regulates genes that are not part of this cell rescue program, and the induction of bacteriophages, the movement of pathogenicity islands, and the expression of virulence factors and bacteriocins are all controlled by this important transcription factor. Recently it has emerged that when regulating the expression of genes from mobile genetic elements (MGEs), LexA often does so in concert with a corepressor. This accessory regulator can either be a host-encoded global transcription factor, which responds to various metabolic changes, or a factor that is encoded for by the MGE itself. Thus, the coupling of LexA-mediated regulation to a secondary transcription factor not only detaches LexA from its primary SOS role, but also fine-tunes gene expression from the MGE, enabling it to respond to multiple stresses. Here we discuss the mechanisms of such coordinated regulation and its implications for cells carrying such MGEs.

摘要

SOS 反应是细菌应对 DNA 损伤的一个重要过程。SOS 基因的表达受 LexA 控制,LexA 是一种全局转录因子,在应激下会自我切割,从而允许表达 DNA 修复功能,并延迟细胞分裂,直到损伤得到修复。LexA 还调节不属于该细胞救援程序的基因,噬菌体的诱导、致病性岛的移动以及毒力因子和细菌素的表达都受这个重要的转录因子控制。最近的研究表明,在调节移动遗传元件 (MGEs) 上的基因表达时,LexA 通常与一个核心抑制剂协同作用。这种辅助调节剂可以是宿主编码的全局转录因子,它响应各种代谢变化,也可以是 MGE 本身编码的因子。因此,LexA 介导的调节与二级转录因子的偶联不仅使 LexA 脱离其主要的 SOS 作用,而且还能从 MGE 上微调基因表达,使其能够应对多种应激。在这里,我们讨论了这种协调调节的机制及其对携带这种 MGE 的细胞的影响。

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