Occurrence and repair of alkylating stress in the intracellular pathogen Brucella abortus

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作者
Katy Poncin
Agnès Roba
Ravikumar Jimmidi
Georges Potemberg
Antonella Fioravanti
Nayla Francis
Kévin Willemart
Nicolas Zeippen
Arnaud Machelart
Emanuele G. Biondi
Eric Muraille
Stéphane P. Vincent
Xavier De Bolle
机构
[1] URBM,Sir William Dunn School of Pathology
[2] Narilis,Unité de Chimie Organique
[3] University of Namur,Unité de Glycobiologie Structurale et Fonctionnelle
[4] University of Oxford,Université de Lille, CNRS, INSERM, CHU Lille, Institut Pasteur de Lille, U1019, UMR 8204
[5] University of Namur,Laboratoire de Parasitologie, Faculté de Médecine
[6] UMR 8576 CNRS,undefined
[7] Université de Lille,undefined
[8] VIB,undefined
[9] Vrije Universiteit Brussel,undefined
[10] Center for Infection and Immunity of Lille,undefined
[11] IMM,undefined
[12] 31 Chemin Joseph Aiguier,undefined
[13] 13009 Marseille,undefined
[14] Aix-Marseille Université,undefined
[15] Université Libre de Bruxelles,undefined
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摘要
It is assumed that intracellular pathogenic bacteria have to cope with DNA alkylating stress within host cells. Here we use single-cell reporter systems to show that the pathogen Brucella abortus does encounter alkylating stress during the first hours of macrophage infection. Genes encoding direct repair and base-excision repair pathways are required by B. abortus to face this stress in vitro and in a mouse infection model. Among these genes, ogt is found to be under the control of the conserved cell-cycle transcription factor GcrA. Our results highlight that the control of DNA repair in B. abortus displays distinct features that are not present in model organisms such as Escherichia coli.
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