Herd immunity underlies homologous recombination in stationary phase bacteria.

Homologous recombination is ubiquitous across evolution, generating variation through genetic reshuffling. Although bacteria lack meiotic recombination, homologous recombination has been known to extensively shape their genomes. However, the mechanisms and ecological conditions sustaining frequent recombination in bacteria remain unclear. Using an Escherichia coli - P1 phage model system, we reveal how frequent recombination emerges from CRISPR-based herd immunity to a generalized transducing phage (DNA vector). Herd immunity maintains phage-susceptible donor bacteria, recipient immune bacteria, and transducing phage, which promotes chromosomal gene flow that exceeds spontaneous mutation by up to two orders of magnitude. Notably, recombination begins as bacterial cultures enter stationary phase, when canonical mutation supply through population growth and DNA replication is strongly reduced, and recombination can be reinitiated by brief fresh nutrient pulses. Genetic analysis showed that stationary-phase recombination requires recA, recB, and recG, connecting this process to a defined homologous-recombination pathway, and suggests a plausible transcriptional regulatory link to transition to nutrient limitation. Bacterial herd immunity therefore has an unexpected evolutionary consequence: it can promote homologous recombination by turning phages into de facto pollinators. This mechanism can help explain how high rates of homologous recombination may be sustained across bacterial populations and suggests that bacterial immune systems can shape molecular evolution not only by blocking infection, but also by regulating genetic exchange.