title: SOS response activation and competence development are antagonistic mechanisms in Streptococcus thermophilus.
abstract: Streptococcus includes species that either contain or lack the LexA-like repressor (HdiR) of the classical SOS response. In Streptococcus pneumoniae, a species which belongs to the latter group, SOS response inducers (e.g., mitomycin C [Mc] and fluoroquinolones) were shown to induce natural transformation, leading to the hypothesis that DNA damage-induced competence could contribute to genomic plasticity and stress resistance. Using reporter strains and microarray experiments, we investigated the impact of the SOS response inducers mitomycin C and norfloxacin and the role of HdiR on competence development in Streptococcus thermophilus. We show that both the addition of SOS response inducers and HdiR inactivation have a dual effect, i.e., induction of the expression of SOS genes and reduction of transformability. Reduction of transformability results from two different mechanisms, since HdiR inactivation has no major effect on the expression of competence (com) genes, while mitomycin C downregulates the expression of early and late com genes in a dose-dependent manner. The downregulation of com genes by mitomycin C was shown to take place at the level of the activation of the ComRS signaling system by an unknown mechanism. Conversely, we show that a ComX-deficient strain is more resistant to mitomycin C and norfloxacin in a viability plate assay, which indicates that competence development negatively affects the resistance of S. thermophilus to DNA-damaging agents. Altogether, our results strongly suggest that SOS response activation and competence development are antagonistic processes in S. thermophilus.
authors.affiliation: Biochimie et Génétique Moléculaire Bactérienne, Institut des Sciences de la Vie, Université Catholique de Louvain, Louvain-la-Neuve, Belgium.
authors.forename: Céline
authors.initials: C
authors.lastname: Boutry
authors.forename: Brigitte
authors.initials: B
authors.lastname: Delplace
authors.forename: André
authors.initials: A
authors.lastname: Clippe
authors.forename: Laetitia
authors.initials: L
authors.lastname: Fontaine
authors.forename: Pascal
authors.initials: P
authors.lastname: Hols
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D004249:DNA Damage; D061269:DNA Transformation Competence / Q000502:physiology*; D017353:Gene Deletion; D015964:Gene Expression Regulation, Bacterial / Q000502:physiology*; D017930:Genes, Reporter; D016685:Mitomycin / Q000494:pharmacology; D008969:Molecular Sequence Data; D020411:Oligonucleotide Array Sequence Analysis; D012329:RNA, Bacterial; D013014:SOS Response, Genetics / Q000502:physiology*; D015398:Signal Transduction; D013045:Species Specificity; D048249:Streptococcus thermophilus / Q000378:metabolism*; D059467:Transcriptome
chemical_list: D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D012329:RNA, Bacterial; D016685:Mitomycin