Quorum sensing is a density-dependent form of communication in bacteria. In streptococci, the quorum sensing system sil (streptococcal invasion locus) has been associated with virulence and bacteriocin production [1], [2], [3]. In this system, the autoinducing peptide SilCR is sensed by histidine kinase SilB, which as a response regulator phosphorylates transcription activator SilA. SilA alters gene expression, causing an increased expression of all sil genes, including silCR. SilCR is excreted and processed by SilD and SilE [2], [4]. In Streptococcus anginosus, sil regulates the expression of Angicin, a bacteriocin active against various streptococci, listeria and enterococci [3].
To further characterize the sil system in S. anginosus, deletion mutants of all sil genes were constructed and investigated for their influence on Angicin production. In most strains, the deletion of any gene led to a loss of antimicrobial activity. While a supplementation with synthetic SilCR restored the inhibitory activity of the silCR deletion mutant, it had no effect on any of the other mutants. To assess the role of sil for bacterial fitness, a sil deletion mutant was compared to the wildtype strain in coculture with rival species. In this setting, the bacteriocin producing wildtype strain demonstrated a significantly enhanced survival, outperforming the sil deletion mutant.
Our study is the first to functionally characterize the sil system of S. anginosus, highlighting its crucial role in bacteriocin production and intra- and interspecies competition.