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Article

Tight Interplay between Replication Stress and Competence Induction in Streptococcus pneumoniae

by 1,2,†, 1,2,† and 1,2,*
1
Laboratoire de Microbiologie et Génétique Moléculaires (LMGM), Centre de Biologie Integrative (CBI), Centre National de la Recherche Scientifique (CNRS), 31062 Toulouse, France
2
Université de Toulouse, Université Paul Sabatier, 31062 Toulouse, France
*
Author to whom correspondence should be addressed.
These authors equally contributed to this work.
Academic Editors: Bernard S. Lopez and Ivan Matic
Cells 2021, 10(8), 1938; https://doi.org/10.3390/cells10081938
Received: 28 May 2021 / Revised: 15 July 2021 / Accepted: 20 July 2021 / Published: 30 July 2021
Cells respond to genome damage by inducing restorative programs, typified by the SOS response of Escherichia coli. Streptococcus pneumoniae (the pneumococcus), with no equivalent to the SOS system, induces the genetic program of competence in response to many types of stress, including genotoxic drugs. The pneumococcal competence regulon is controlled by the origin-proximal, auto-inducible comCDE operon. It was previously proposed that replication stress induces competence through continued initiation of replication in cells with arrested forks, thereby increasing the relative comCDE gene dosage and expression and accelerating the onset of competence. We have further investigated competence induction by genome stress. We find that absence of RecA recombinase stimulates competence induction, in contrast to SOS response, and that double-strand break repair (RexB) and gap repair (RecO, RecR) initiation effectors confer a similar effect, implying that recombinational repair removes competence induction signals. Failure of replication forks provoked by titrating PolC polymerase with the base analogue HPUra, over-supplying DnaA initiator, or under-supplying DnaE polymerase or DnaC helicase stimulated competence induction. This induction was not correlated with concurrent changes in origin-proximal gene dosage. Our results point to arrested and unrepaired replication forks, rather than increased comCDE dosage, as a basic trigger of pneumococcal competence. View Full-Text
Keywords: DNA damage response; genome integrity; replication stress; recombinational repair; bacterial competence; Streptococcus pneumoniae DNA damage response; genome integrity; replication stress; recombinational repair; bacterial competence; Streptococcus pneumoniae
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MDPI and ACS Style

Khemici, V.; Prudhomme, M.; Polard, P. Tight Interplay between Replication Stress and Competence Induction in Streptococcus pneumoniae. Cells 2021, 10, 1938. https://doi.org/10.3390/cells10081938

AMA Style

Khemici V, Prudhomme M, Polard P. Tight Interplay between Replication Stress and Competence Induction in Streptococcus pneumoniae. Cells. 2021; 10(8):1938. https://doi.org/10.3390/cells10081938

Chicago/Turabian Style

Khemici, Vanessa, Marc Prudhomme, and Patrice Polard. 2021. "Tight Interplay between Replication Stress and Competence Induction in Streptococcus pneumoniae" Cells 10, no. 8: 1938. https://doi.org/10.3390/cells10081938

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