Year: 2025
Type: preprint
Abstract: In bacteria, defense against predators and competitors often requires cooperation within large clonal bacterial populations. Mutations that inactivate biosynthesis of costly molecules involved in cooperative defense can increase the growth rate of the mutants, while mutant cells continue to benefit from the efforts of wild type cells. The GacA-GacS signaling pathway regulates biosynthesis and secretion of toxic secondary metabolites and proteins that play crucial roles in bacterial defense in Pseudomonas species, including resistance to the protozoan predator Dictyostelium discoideum . A P. protegens Δ gacA mutant is vulnerable to predation but can benefit from protection provided by wild type cells in mixed populations. Wild type P. protegens sporadically infects D. discoideum fruiting bodies which may aid in bacterial dispersal to new environments. We found that the Δ gacA mutant does not infect fruiting bodies and that the wild type does not infect when at low abundance in the population. The P. protegens ΔgacA mutant is a cheater whose fitness under predation depends on its relative abundance. Protozoan predators can limit the abundance of Δ gacA mutants in Pseudomonas populations, preventing selective sweeps that could lead to the loss of the important but costly Gac regulon.
Institutions: Texas Tech University, Washington University in St. Louis
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
Funder: National Science Foundation
OpenAlex ID: W4416046986