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Marvig, R. L.

Publications and source records attributed to Marvig, R. L..

2 recordsLinked to original sources

Privatisation rescues function following loss of cooperation

A single cheating mutant can lead to the invasion and eventual eradication of cooperation from a population. Consequently, cheat invasion is often considered as \"game over\" in empirical and theoretical studies of cooperator-cheat dynamics, especially when cooperation is necessary for fulfilling an essential function. But is cheat invasion necessarily \"game over\" in nature? By following a population of bacteria through loss of cooperation and beyond, we observed that individuals evolved to replace cooperation with a selfish, or \"private\" behaviour. Specifically, we show that when cheating caused the loss of cooperative iron acquisition in a collection of Pseudomonas aeruginosa isolates from cystic fibrosis patients, a private uptake system that only benefits the focal individual was upregulated. This observation highlights the importance of social dynamics of natural populations and emphasizes the potential impact of past social interaction on the evolution of private traits.

evolutionary biology

Virulence evolution in the opportunistic bacterial pathogen Pseudomonas aeruginosa

Bacterial opportunistic pathogens are feared for their difficult-to-treat nosocomial infections and for causing morbidity in immunocompromised patients. Here, we study how such a versatile opportunist, Pseudomonas aeruginosa, adapts to conditions inside and outside its model host Caenorhabditis elegans, and use phenotypic and genotypic screens to identify the mechanistic basis of virulence evolution. We found that virulence significantly dropped in unstructured environments both in the presence and absence of the host, but remained unchanged in spatially structured environments. Reduction of virulence was either driven by a substantial decline in the production of siderophores (in treatments without hosts) or toxins and proteases (in treatments with hosts). Whole-genome sequencing of evolved clones revealed positive selection and parallel evolution across replicates, and showed an accumulation of mutations in regulator genes controlling virulence factor expression. Our study identifies the spatial structure of the non-host environment as a key driver of virulence evolution in an opportunistic pathogen.

microbiology