Líffræðifélag Íslands - biologia.is
Líffræðiráðstefnan 2025
Erindi/veggspjald / Talk/poster E111
Höfundar / Authors: Ilmur Jónsdóttir (1), Andrew T Nishimoto (1), Haley Echlin (1), Nadia Olivero (1), Abigail McKnight (1), Amy Iverson (1), & Jason W Rosch (1)
Starfsvettvangur / Affiliations: 1. Department of Host-Microbe Interactions, St. Jude Children’s Research Hospital, Memphis, Tennessee, USA
Kynnir / Presenter: Ilmur Jónsdóttir
Bacterial pathogens continually evolve to overcome stressors such as antibiotics, posing a major threat to public health. Recently we found a novel adaptive mechanism in Streptococcus pneumoniae and in other pathogens, termed recombination-associated mutagenesis (RAM). Unlike generalized stress responses, RAM generates a distinct mutational signature localized specifically to sites of homologous recombination. This process drives the emergence of de novo antimicrobial resistance (AMR) mutations. Mechanistically, we link RAM to the activity of error-prone polymerases DinB and DnaE. Intriguingly, RAM appears conserved in other clinically relevant pathogens, including Acinetobacter baumannii, but is absent in species possessing a canonical SOS response regulated by LexA, which both S. pneumoniae and A. baumannii lack. Our findings reveal a stress-induced, recombination-coupled mutagenesis program distinct from the SOS response, highlighting a previously unappreciated route to AMR evolution in key pathogens and pointing to new targets for limiting resistance development.