Contact-dependent growth inhibition drives kin discrimination and shapes in vivo strain dominance in Pseudomonas aeruginosa infection
- 1Loyola University Chicago Stritch School of Medicine
Abstract
Pseudomonas aeruginosa is a ubiquitous environmental bacterium and an opportunistic pathogen. Rather than existing as single clonal lineages, environmental and clinical populations often consist of a mixture of distinct strains that directly compete to dominate the niche. To eliminate rivals, P. aeruginosa deploys a form of interference competition termed contact-dependent growth inhibition (CDI). CDI is mediated by CdiA, where, upon cell contact, the CdiA C-terminal toxin domain is delivered to prey cells. Toxin-producing cells encode for a cognate CdiI immunity protein to prevent self-intoxication. Different strains of P. aeruginosa encode for CdiA proteins with different C-terminal toxin domains and cognate CdiI immunity proteins. Most studies have relied on engineered strains to investigate the mechanism of CDI. While extremely useful for studying CdiA-mediated intoxication, such work masks the true diversity of wild-type CdiA variants and their impact on competitive interactions between strains. In this study, we systematically investigated CDI-mediated competition using unique conspecific strains of P. aeruginosa. We identified several novel CdiA toxin domains and mapped the competitive outcomes they govern. Furthermore, using a mouse model of acute pneumonia, we demonstrate that CDI-mediated interference competition actively occurs during mixed-strain infections in vivo. Together, our findings reveal that P. aeruginosa leverages CDI as a potent, strain-dependent kin discrimination mechanism that directly shapes population dynamics and strain dominance within host and natural environments.
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BibTeX
@misc{peterson2026contactdependent,
title = {{Contact-dependent growth inhibition drives kin discrimination and shapes in vivo strain dominance in Pseudomonas aeruginosa infection}},
author = {N. Peterson and B. Cobe and A. Bronson and J. Allen},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.30.755834},
url = {https://www.biorxiv.org/content/10.64898/2026.09.30.755834v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Contact-dependent growth inhibition drives kin discrimination and shapes in vivo strain dominance in Pseudomonas aeruginosa infection
AU - N. Peterson
AU - B. Cobe
AU - A. Bronson
AU - J. Allen
PY - 2026
DA - 2026/09/30
PB - bioRxiv
DO - 10.64898/2026.09.30.755834
UR - https://www.biorxiv.org/content/10.64898/2026.09.30.755834v1
AB - Pseudomonas aeruginosa is a ubiquitous environmental bacterium and an opportunistic pathogen. Rather than existing as single clonal lineages, environmental and clinical populations often consist of a mixture of distinct strains that directly compete to dominate the niche. To eliminate rivals, P. aeruginosa deploys a form of interference competition termed contact-dependent growth inhibition (CDI). CDI is mediated by CdiA, where, upon cell contact, the CdiA C-terminal toxin domain is delivered to prey cells. Toxin-producing cells encode for a cognate CdiI immunity protein to prevent self-intoxication. Different strains of P. aeruginosa encode for CdiA proteins with different C-terminal toxin domains and cognate CdiI immunity proteins. Most studies have relied on engineered strains to investigate the mechanism of CDI. While extremely useful for studying CdiA-mediated intoxication, such work masks the true diversity of wild-type CdiA variants and their impact on competitive interactions between strains. In this study, we systematically investigated CDI-mediated competition using unique conspecific strains of P. aeruginosa. We identified several novel CdiA toxin domains and mapped the competitive outcomes they govern. Furthermore, using a mouse model of acute pneumonia, we demonstrate that CDI-mediated interference competition actively occurs during mixed-strain infections in vivo. Together, our findings reveal that P. aeruginosa leverages CDI as a potent, strain-dependent kin discrimination mechanism that directly shapes population dynamics and strain dominance within host and natural environments.
ER -