Granato, E. T. | Search bioRxiv

bioRxiv2018

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↗

bioRxiv2017

The path to re-evolve cooperation is constrained in Pseudomonas aeruginosa

BackgroundA common form of cooperation in bacteria is based on the secretion of beneficial metabolites, shareable as public good among cells at the group level. Because cooperation can be exploited by \"cheat\" mutants, which contribute less or nothing to the public good, there has been great interest in understanding the conditions required for cooperation to remain evolutionarily stable. In contrast, much less is known about whether cheats, once fixed in the population, are able to revert back to cooperation when conditions change. Here, we tackle this question by subjecting experimentally evolved cheats of Pseudomonas aeruginosa, partly deficient for the production of the iron-scavenging public good pyoverdine, to conditions previously shown to favor cooperation.\n\nResultsFollowing approximately 200 generations of experimental evolution, we screened 720 evolved clones for changes in their pyoverdine production levels. We found no evidence for the re-evolution of full cooperation, even in environments with increased spatial structure, and reduced costs of cooperation - two conditions that have previously been shown to maintain cooperation. In contrast, we observed selection for complete abolishment of pyoverdine production. The patterns of complete trait degradation were likely driven by \"cheating on cheats\" in unstructured, iron-limited environments where pyoverdine is important for growth, and selection against a maladaptive trait in iron-rich environments where pyoverdine is superfluous.\n\nConclusionsOur study shows that the path to re-evolve cooperation seems constrained. One reason might be that the number of mutational targets potentially leading to reversion is limited. Alternatively, it could be that the selective conditions required for revertants to spread from rare are much more stringent than those needed to maintain cooperation.

evolutionary biology↗