@article{23090,
  abstract     = {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.},
  author       = {Payne, Pavel and Plevka, Pavel and Bollback, Jonathan P and Guet, Calin C},
  issn         = {1537-1719},
  journal      = {Molecular Biology and Evolution},
  keywords     = {homologous recombination, defense systems, CRISPR-Cas, herd immunity, stationary phase, bacterial evolution},
  number       = {10},
  publisher    = {Oxford University Press},
  title        = {{Herd immunity underlies homologous recombination in stationary phase bacteria}},
  doi          = {10.1093/molbev/msag238},
  volume       = {43},
  year         = {2026},
}

@misc{9840,
  abstract     = {Herd immunity, a process in which resistant individuals limit the spread of a pathogen among susceptible hosts has been extensively studied in eukaryotes. Even though bacteria have evolved multiple immune systems against their phage pathogens, herd immunity in bacteria remains unexplored. Here we experimentally demonstrate that herd immunity arises during phage epidemics in structured and unstructured Escherichia coli populations consisting of differing frequencies of susceptible and resistant cells harboring CRISPR immunity. In addition, we develop a mathematical model that quantifies how herd immunity is affected by spatial population structure, bacterial growth rate, and phage replication rate. Using our model we infer a general epidemiological rule describing the relative speed of an epidemic in partially resistant spatially structured populations. Our experimental and theoretical findings indicate that herd immunity may be important in bacterial communities, allowing for stable coexistence of bacteria and their phages and the maintenance of polymorphism in bacterial immunity.},
  author       = {Payne, Pavel and Geyrhofer, Lukas and Barton, Nicholas H and Bollback, Jonathan P},
  publisher    = {Dryad},
  title        = {{Data from: CRISPR-based herd immunity limits phage epidemics in bacterial populations}},
  doi          = {10.5061/dryad.42n44},
  year         = {2018},
}

@article{423,
  abstract     = {Herd immunity, a process in which resistant individuals limit the spread of a pathogen among susceptible hosts has been extensively studied in eukaryotes. Even though bacteria have evolved multiple immune systems against their phage pathogens, herd immunity in bacteria remains unexplored. Here we experimentally demonstrate that herd immunity arises during phage epidemics in structured and unstructured Escherichia coli populations consisting of differing frequencies of susceptible and resistant cells harboring CRISPR immunity. In addition, we develop a mathematical model that quantifies how herd immunity is affected by spatial population structure, bacterial growth rate, and phage replication rate. Using our model we infer a general epidemiological rule describing the relative speed of an epidemic in partially resistant spatially structured populations. Our experimental and theoretical findings indicate that herd immunity may be important in bacterial communities, allowing for stable coexistence of bacteria and their phages and the maintenance of polymorphism in bacterial immunity.},
  author       = {Payne, Pavel and Geyrhofer, Lukas and Barton, Nicholas H and Bollback, Jonathan P},
  journal      = {eLife},
  publisher    = {eLife Sciences Publications},
  title        = {{CRISPR-based herd immunity can limit phage epidemics in bacterial populations}},
  doi          = {10.7554/eLife.32035},
  volume       = {7},
  year         = {2018},
}

@phdthesis{6291,
  abstract     = {Bacteria and their pathogens – phages – are the most abundant living entities on Earth. Throughout their coevolution, bacteria have evolved multiple immune systems to overcome the ubiquitous threat from the phages. Although the molecu- lar details of these immune systems’ functions are relatively well understood, their epidemiological consequences for the phage-bacterial communities have been largely neglected. In this thesis we employed both experimental and theoretical methods to explore whether herd and social immunity may arise in bacterial popu- lations. Using our experimental system consisting of Escherichia coli strains with a CRISPR based immunity to the T7 phage we show that herd immunity arises in phage-bacterial communities and that it is accentuated when the populations are spatially structured. By fitting a mathematical model, we inferred expressions for the herd immunity threshold and the velocity of spread of a phage epidemic in partially resistant bacterial populations, which both depend on the bacterial growth rate, phage burst size and phage latent period. We also investigated the poten- tial for social immunity in Streptococcus thermophilus and its phage 2972 using a bioinformatic analysis of potentially coding short open reading frames with a signalling signature, encoded within the CRISPR associated genes. Subsequently, we tested one identified potentially signalling peptide and found that its addition to a phage-challenged culture increases probability of survival of bacteria two fold, although the results were only marginally significant. Together, these results demonstrate that the ubiquitous arms races between bacteria and phages have further consequences at the level of the population.},
  author       = {Payne, Pavel},
  issn         = {2663-337X},
  pages        = {83},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{Bacterial herd and social immunity to phages}},
  year         = {2017},
}