Convergent Evolution of Competitive Fitness via Quorum Sensing Disruption in Bacillus subtilis
Intraspecies competition shapes microbial community structure and             evolution, yet the mechanisms determining competitive outcomes among             closely related strains remain unclear. The soil bacterium Bacillus             subtilis is a model for microbial social interactions, where             quorum-sensing systems regulate cooperation and antagonism. Strain NCIB             3610 carries an atypical RapP-PhrP module that alters quorum-sensing             control and promotes faster growth. Here, we combine mathematical             modelling, genetic reconstruction, experimental evolution,             transcriptomics, and comparative genomics to dissect the role of             quorum-sensing regulation in competitive fitness. Modelling and mutant             analysis demonstrate that small differences in growth rate conferred by             RapP-PhrP3610 can be sufficient to drive competitive exclusion.             Experimental evolution of distinct wild isolates revealed recurrent             mutations in the sensor kinase comP, which phenocopy complete comP or comA             deletions and confer a growth-linked competitive advantage. A phylogenomic             survey of 370 B. subtilis genomes identified disruptive comP mutations in             ~16% of isolates, including a hotspot within a poly-thymidine tract             enriched in strains sharing the NCIB 3610 pherotype. However, growth rate             alone does not explain all interaction outcomes as even isogenic strains             with equivalent doubling times differ in competitiveness. Transcriptomic             profiling implicates a type VII secretion system toxin as an additional             effector. Together, these findings reveal that disruption of             quorum-sensing pathways, whether naturally or through selection, provides             a rapid route to competitive advantage, highlighting a fundamental             trade-off between communal signaling and individual fitness in microbial             populations.