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()的失活会诱导SOS反应和移动遗传元件的动员,并使()中的一般应激反应和毒力程序沉默。

Inactivation of () induces the SOS response and MGEs mobilization and silences the general stress response and virulence program in .

作者信息

Ładziak Magdalena, Prochwicz Emilia, Gut Karina, Gomza Patrycja, Jaworska Karolina, Ścibek Katarzyna, Młyńska-Witek Marta, Kadej-Zajączkowska Katarzyna, Lillebaek Eva M S, Kallipolitis Birgitte H, Krawczyk-Balska Agata

机构信息

Department of Molecular Microbiology, Biological and Chemical Research Centre, Faculty of Biology, University of Warsaw, Warsaw, Poland.

Department of Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark.

出版信息

Front Microbiol. 2024 Jan 4;14:1324062. doi: 10.3389/fmicb.2023.1324062. eCollection 2023.

Abstract

Bacteria have evolved numerous regulatory pathways to survive in changing environments. The SOS response is an inducible DNA damage repair system that plays an indispensable role in bacterial adaptation and pathogenesis. Here we report a discovery of the previously uncharacterized protein Lmo0946 as an SOS response interfering factor (Sif) in the human pathogen Functional genetic studies demonstrated that is indispensable for normal growth of in stress-free as well as multi-stress conditions, and contributes to susceptibility to β-lactam antibiotics, biofilm formation and virulence. Absence of Sif promoted the SOS response and elevated expression of mobilome genes accompanied by mobilization of the A118 prophage and ICELm-1 mobile genetic elements (MGEs). These changes were found to be associated with decreased expression of general stress response genes from the σB regulon as well as virulence genes, including the PrfA regulon. Together, this study uncovers an unexpected role of a previously uncharacterized factor, Sif, as an inhibitor of the SOS response in .

摘要

细菌已经进化出多种调控途径以在不断变化的环境中生存。SOS反应是一种可诱导的DNA损伤修复系统,在细菌适应和致病过程中发挥着不可或缺的作用。在此,我们报告发现了以前未被表征的蛋白质Lmo0946作为人类病原体中的SOS反应干扰因子(Sif)。功能遗传学研究表明,Sif对于该病原体在无应激以及多应激条件下的正常生长不可或缺,并且它会导致对β-内酰胺抗生素的敏感性增加、生物膜形成及毒力增强。缺乏Sif会促进SOS反应并提高移动基因组基因的表达,同时伴随着A118原噬菌体和ICELm-1移动遗传元件(MGEs)的移动。这些变化被发现与来自σB调控子的一般应激反应基因以及包括PrfA调控子在内的毒力基因的表达降低有关。总之,这项研究揭示了一个以前未被表征的因子Sif作为该病原体中SOS反应抑制剂的意想不到的作用。

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