Open AccessCinA is regulated via ComX to modulate genetic transformation and cell viability in S treptococcus mutans
Author(s) -
Mair Richard W.,
Senadheera Dilani B.,
Cvitkovitch Dennis G.
Publication year - 2012
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2012.02550.x
Subject(s) - regulon , complementation , biology , mutant , streptococcus mutans , operon , gene , mutagenesis , phenotype , genetics , microbiology and biotechnology , bacteria
The S treptococcus mutans ComX ‐regulon encompasses > 200 mostly uncharacterized genes, including cinA . Here we report that cinA is regulated by ComX in the presence of the competence stimulating peptide ( CSP ), wherein loss of CinA (strain SmuCinA ) results in reduced transformability with or without added CSP by 74‐ and 15‐fold, respectively ( P < 0.003). In CSP ‐supplemented cultures, a two‐fold increase in cell viability was noted for SmuCinA relative to UA 159 ( P < 0.002), suggesting CinA 's involvement in the CSP ‐modulated cell killing response. Relative to UA 159, loss of CinA also rendered the mutant hypersensitive to killing by methyl methanesulfonate ( MMS ), which impairs homologous recombination. Despite our use of a non‐polar mutagenesis strategy to knockout cinA , which is the first gene of the multicistronic operon harboring cinA , we noted a drastic reduction in recA expression. By using a CinA ‐complemented mutant, we were able to partially, but not completely restore all phenotypes to UA 159 levels. Complementation results suggested that although cinA participates in modulating competence, viability and MMS tolerance, genes downstream of the cinA transcript may also regulate these phenotypes, a finding that warrants further examination. This is the first report that describes a role for S . mutans ' CinA in contending with DNA damage, genetic transformation and cell survival.