In:
PLOS Genetics, Public Library of Science (PLoS), Vol. 18, No. 5 ( 2022-5-25), p. e1010198-
Abstract:
Competence for DNA transformation is a major strategy for bacterial adaptation and survival. Yet, this successful tactic is energy-consuming, shifts dramatically the metabolism, and transitory impairs the regular cell-cycle. In streptococci, complex regulatory pathways control competence deactivation to narrow its development to a sharp window of time, a process known as competence shut-off. Although characterized in streptococci whose competence is activated by the ComCDE signaling pathway, it remains unclear for those controlled by the ComRS system. In this work, we investigate competence shut-off in the major human gut commensal Streptococcus salivarius . Using a deterministic mathematical model of the ComRS system, we predicted a negative player under the control of the central regulator ComX as involved in ComS/XIP pheromone degradation through a negative feedback loop. The individual inactivation of peptidase genes belonging to the ComX regulon allowed the identification of PepF as an essential oligoendopeptidase in S . salivarius . By combining conditional mutants, transcriptional analyses, and biochemical characterization of pheromone degradation, we validated the reciprocal role of PepF and XIP in ComRS shut-off. Notably, engineering cleavage site residues generated ultra-resistant peptides producing high and long-lasting competence activation. Altogether, this study reveals a proteolytic shut-off mechanism of competence in the salivarius group and suggests that this mechanism could be shared by other ComRS-containing streptococci.
Type of Medium:
Online Resource
ISSN:
1553-7404
DOI:
10.1371/journal.pgen.1010198
DOI:
10.1371/journal.pgen.1010198.g001
DOI:
10.1371/journal.pgen.1010198.g002
DOI:
10.1371/journal.pgen.1010198.g003
DOI:
10.1371/journal.pgen.1010198.g004
DOI:
10.1371/journal.pgen.1010198.g005
DOI:
10.1371/journal.pgen.1010198.g006
DOI:
10.1371/journal.pgen.1010198.g007
DOI:
10.1371/journal.pgen.1010198.s001
DOI:
10.1371/journal.pgen.1010198.s002
DOI:
10.1371/journal.pgen.1010198.s003
DOI:
10.1371/journal.pgen.1010198.s004
DOI:
10.1371/journal.pgen.1010198.s005
DOI:
10.1371/journal.pgen.1010198.s006
DOI:
10.1371/journal.pgen.1010198.s007
DOI:
10.1371/journal.pgen.1010198.s008
DOI:
10.1371/journal.pgen.1010198.s009
DOI:
10.1371/journal.pgen.1010198.s010
DOI:
10.1371/journal.pgen.1010198.s011
DOI:
10.1371/journal.pgen.1010198.s012
DOI:
10.1371/journal.pgen.1010198.s013
DOI:
10.1371/journal.pgen.1010198.s014
DOI:
10.1371/journal.pgen.1010198.s015
DOI:
10.1371/journal.pgen.1010198.s016
DOI:
10.1371/journal.pgen.1010198.s017
DOI:
10.1371/journal.pgen.1010198.s018
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2022
detail.hit.zdb_id:
2186725-2
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