Tight Interplay between Replication Stress and Competence Induction in Streptococcus pneumoniae

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.