PubMed · 16097662
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B W Holloway, V Krishnapillai, V Stanisich. 1971. Pseudomonas genetics.. https://doi.org/10.1146/annurev.ge.05.120171.002233
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UNLABELLED: Streptococcus pneumoniae is a major colonizer of the human nasopharynx, where inter- and intra-strain competition plays a critical role in shaping population structure and influencing vaccine outcomes. Bacteriocins are key mediators of intra-species competition, yet many of their functions and regulatory mechanisms remain poorly understood. Here, we identify and characterize streptolancidin D, a previously uncharacterized bacteriocin encoded by the sldA-T locus, and demonstrate its contribution to pneumococcal competition. Using isogenic streptolancidin-producing and non-producing variants of a naturally colonizing strain, we show that sldA-T contributes to the inhibition of competitor strains in in vitro biofilms and during murine co-colonization. Importantly, streptolancidin D also inhibited in vitro a subset of genetically diverse pneumococcal isolates representing multiple serotypes, whereas non-producing variants showed no activity. This indicates that its effect is broad and not restricted to isogenic interactions. Genomic analysis of over 7,500 pneumococcal genomes revealed that sldA-T is present in ~12% of isolates, with lineage-associated distribution patterns, and is consistently encoded downstream of the Rgg144/SHP144 quorum sensing system. We further demonstrate that sldA-T is regulated by this system, with sldA-T promoter activity abolished in a SHP-deficient background and partially restored by exogenous peptide stimulation. Finally, we show that streptolancidin D acts in concert with other bacteriocin systems and competence-mediated fratricide, highlighting a multifactorial antimicrobial strategy that enhances pneumococcal competitiveness. Overall, our findings identify a quorum sensing-regulated bacteriocin that contributes to pneumococcal competition and helps shape population dynamics. IMPORTANCE: Bacteriocins are central to bacterial competition and niche occupation, particularly in structured environments like the human nasopharynx. While several pneumococcal bacteriocins have been characterized, the functions of many remain unknown, limiting our understanding of how these systems shape strain fitness and population dynamics. We characterize streptolancidin D, a bacteriocin that enhances intraspecies competitiveness in vitro and in vivo and contributes to the inhibition of genetically diverse pneumococcal strains. We demonstrate that its expression is tightly regulated by the conserved Rgg144/SHP144 quorum sensing system and that the locus is distributed and shows synteny across multiple pneumococcal lineages. Our findings reveal that streptolancidin D operates within a broader network of bacteriocins and competence-associated mechanisms that collectively shape competitive interactions. By integrating genomic, functional, and regulatory analyses, this work expands the known repertoire of pneumococcal antimicrobial systems and provides new insights into the mechanisms underpinning competition and population structure in S. pneumoniae.
Unmodified class II bacteriocins promise precision antimicrobials that spare bystander microbes. Zhang and colleagues introduce IIBacFinder, a genomics-guided pipeline that detects precursor and context genes with a curated pHMM library, infers leader-peptide cleavage, and triages candidates by meta-omics signals. The authors apply it across bacterial genomes, including an atlas of ∼280,000 human-gut genomes, and recover a vast reservoir of narrow-spectrum peptides and prioritize gut-resident candidates for synthesis. Of the 26 synthesized, 16 display activity in vitro, largely via membrane perturbation and with additive effects alongside vancomycin, while ex vivo assays show minimal compositional disruption of fecal communities compared with antibiotic controls. These results position unmodified class II bacteriocins as tractable, microbiome-sparing agents and illustrate how genome-scale mining coupled to meta-omics can bridge sequence to function in complex ecosystems.
Locally adapted residents present a formidable barrier to invasion . One solution for invaders is to kill residents . Here, we explore the comparative ecological dynamics of two distinct microbial mechanisms of killing competitors, via the release of chemicals (e.g., bacteriocins ) and via the release of parasites (e.g., temperate phage ). We compared the short-term population dynamics of susceptible E. coli K12 and isogenic carriers of phage varphi80 in experimental cultures to that anticipated by mathematical models using independently derived experimental parameters. Whereas phages are a direct burden to their carriers because of probabilistic host lysis, by killing competitor bacteria they can indirectly benefit bacterial kin made immune by carrying isogenic phage. This is similar to previously described bacteriocin-mediated effects. However, unlike chemical killing, viable phage trigger an epidemic among susceptible competitors, which become factories producing more phage. Amplification makes phage carriers able to invade well-mixed susceptibles even faster when rare, whereas chemical killers can only win in a well-mixed environment when sufficiently abundant. We demonstrate that for plausible parameters, the release of chemical toxins is superior as a resident strategy to repel invasions, whereas the release of temperate phage is superior as a strategy of invasion.