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Related Experiment Video

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Tight Interplay between Replication Stress and Competence Induction in Streptococcus pneumoniae.

Vanessa Khemici1,2, Marc Prudhomme1,2, Patrice Polard1,2

  • 1Laboratoire de Microbiologie et Génétique Moléculaires (LMGM), Centre de Biologie Integrative (CBI), Centre National de la Recherche Scientifique (CNRS), 31062 Toulouse, France.

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|August 27, 2021
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Summary

Genome stress in Streptococcus pneumoniae triggers competence via unrepaired replication forks. This contrasts with the SOS response, highlighting a novel stress-induced pathway in bacteria.

Keywords:
DNA damage responseStreptococcus pneumoniaebacterial competencegenome integrityrecombinational repairreplication stress

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • * Cells possess restorative programs for genome damage, like the SOS response in E. coli.
  • * Streptococcus pneumoniae lacks an SOS system but induces competence under stress.
  • * Pneumococcal competence is regulated by the comCDE operon.

Purpose of the Study:

  • * To investigate the mechanism of competence induction by genome stress in Streptococcus pneumoniae.
  • * To determine the role of recombinational repair and replication fork integrity in competence induction.

Main Methods:

  • * Investigated competence induction in Streptococcus pneumoniae mutants lacking RecA, RexB, RecO, or RecR.
  • * Examined competence induction under conditions of replication stress induced by HPUra, DnaA over-supply, or DnaE/DnaC under-supply.
  • * Assessed changes in comCDE gene dosage and expression.

Main Results:

  • * Absence of RecA recombinase and components of double-strand break repair (RexB) and gap repair (RecO, RecR) stimulated competence induction.
  • * Replication fork failure, induced by various methods, strongly stimulated competence.
  • * Competence induction was not correlated with changes in comCDE gene dosage.

Conclusions:

  • * Arrested and unrepaired replication forks are the primary triggers of pneumococcal competence.
  • * Recombinational repair pathways appear to counteract competence induction signals.
  • * This contrasts with the proposed model of increased comCDE gene dosage.