title: The SOS Response Master Regulator LexA Is Associated with Sporulation, Motility and Biofilm Formation in Clostridium difficile.
abstract: The LexA regulated SOS network is a bacterial response to DNA damage of metabolic or environmental origin. In Clostridium difficile, a nosocomial pathogen causing a range of intestinal diseases, the in-silico deduced LexA network included the core SOS genes involved in the DNA repair and genes involved in various other biological functions that vary among different ribotypes. Here we describe the construction and characterization of a lexA ClosTron mutant in C. difficile R20291 strain. The mutation of lexA caused inhibition of cell division resulting in a filamentous phenotype. The lexA mutant also showed decreased sporulation, a reduction in swimming motility, greater sensitivity to metronidazole, and increased biofilm formation. Changes in the regulation of toxin A, but not toxin B, were observed in the lexA mutant in the presence of sub-inhibitory concentrations of levofloxacin. C. difficile LexA is, therefore, not only a regulator of DNA damage but also controls many biological functions associated with virulence.
authors.affiliation: National Laboratory for Health, Environment and Food, NLZOH, Maribor, Slovenia.
authors.forename: Beata M
authors.initials: BM
authors.lastname: Walter
authors.affiliation: The Clostridia Research Group, BBSRC/EPSRC Synthetic Biology Research Centre, School of Life Sciences, Centre for Biomolecular Sciences, University of Nottingham, Nottingham, NG7 2RD, United Kingdom.
authors.forename: Stephen T
authors.initials: ST
authors.lastname: Cartman
authors.affiliation: The Clostridia Research Group, BBSRC/EPSRC Synthetic Biology Research Centre, School of Life Sciences, Centre for Biomolecular Sciences, University of Nottingham, Nottingham, NG7 2RD, United Kingdom.
authors.forename: Nigel P
authors.initials: NP
authors.lastname: Minton
authors.affiliation: Biotechnical Faculty, University of Ljubljana, Department of Biology, Ljubljana, Slovenia.
authors.forename: Matej
authors.initials: M
authors.lastname: Butala
authors.affiliation: National Laboratory for Health, Environment and Food, NLZOH, Maribor, Slovenia.|Faculty of Medicine, University of Maribor, Maribor, Slovenia.|Centre of Excellence for Integrated Approaches in Chemistry and Biology of Proteins, Ljubljana, Slovenia.
authors.forename: Maja
authors.initials: M
authors.lastname: Rupnik
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001426:Bacterial Proteins / Q000235:genetics* / Q000378:metabolism*; D001427:Bacterial Toxins / Q000378:metabolism; D018441:Biofilms / Q000187:drug effects / Q000254:growth & development*; D002455:Cell Division; D016360:Clostridioides difficile / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D004768:Enterotoxins / Q000378:metabolism; D015964:Gene Expression Regulation, Bacterial / Q000187:drug effects; D064704:Levofloxacin / Q000494:pharmacology; D009154:Mutation; D013014:SOS Response, Genetics; D012697:Serine Endopeptidases / Q000235:genetics* / Q000378:metabolism*; D013171:Spores, Bacterial / Q000187:drug effects / Q000254:growth & development; D000099160:LexA Repressor Protein
chemical_list: D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D001427:Bacterial Toxins; D004768:Enterotoxins; D064704:Levofloxacin; D012697:Serine Endopeptidases; D000099160:LexA Repressor Protein; C041348:tcdA protein, Clostridium difficile; C031815:toxB protein, Clostridium difficile