@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},
}

@article{14357,
  abstract     = {Aminoacylation of transfer RNA (tRNA) is a key step in protein biosynthesis, carried out by highly specific aminoacyl-tRNA synthetases (ARSs). ARSs have been implicated in autosomal dominant and autosomal recessive human disorders. Autosomal dominant variants in tryptophanyl-tRNA synthetase 1 (WARS1) are known to cause distal hereditary motor neuropathy and Charcot-Marie-Tooth disease, but a recessively inherited phenotype is yet to be clearly defined. Seryl-tRNA synthetase 1 (SARS1) has rarely been implicated in an autosomal recessive developmental disorder. Here, we report five individuals with biallelic missense variants in WARS1 or SARS1, who presented with an overlapping phenotype of microcephaly, developmental delay, intellectual disability, and brain anomalies. Structural mapping showed that the SARS1 variant is located directly within the enzyme’s active site, most likely diminishing activity, while the WARS1 variant is located in the N-terminal domain. We further characterize the identified WARS1 variant by showing that it negatively impacts protein abundance and is unable to rescue the phenotype of a CRISPR/Cas9 wars1 knockout zebrafish model. In summary, we describe two overlapping autosomal recessive syndromes caused by variants in WARS1 and SARS1, present functional insights into the pathogenesis of the WARS1-related syndrome and define an emerging disease spectrum: ARS-related developmental disorders with or without microcephaly.},
  author       = {Boegershausen, Nina and Krawczyk, Hannah E. and Jamra, Rami A. and Lin, Sheng-Jia and Yigit, Goekhan and Huening, Irina and Polo, Anna M. and Vona, Barbara and Huang, Kevin and Schmidt, Julia and Altmueller, Janine and Luppe, Johannes and Platzer, Konrad and Doergeloh, Beate B. and Busche, Andreas and Biskup, Saskia and Mendes, I, Marisa and Smith, Desiree E. C. and Salomons, Gajja S. and Zibat, Arne and Bueltmann, Eva and Nuernberg, Peter and Spielmann, Malte and Lemke, Johannes R. and Li, Yun and Zenker, Martin and Varshney, Gaurav K. and Hillen, Hauke S. and Kratz, Christian P. and Wollnik, Bernd},
  issn         = {1059-7794},
  journal      = {Human Mutation},
  keywords     = {aminoacylation, aminoacyl-tRNA synthetase, ARS, CRISPR, Cas9, intellectual disability, microcephaly, SARS1, tRNA, WARS1, zebrafish},
  number       = {10},
  pages        = {1454--1471},
  publisher    = {Wiley},
  title        = {{WARS1 and SARS1: Two tRNA synthetases implicated in autosomal recessive microcephaly}},
  doi          = {10.1002/humu.24430},
  volume       = {43},
  year         = {2022},
}