Pyomelanin-producing Pseudomonas aeruginosa selected during chronic infections have a large chromosomal deletion which confers resistance to pyocins

Summary When bacterial lineages make the transition from free‐living to permanent association with hosts, they can undergo massive gene losses, for which the selective forces within host tissues are unknown. We identified here melanogenic clinical isolates of Pseudomonas aeruginosa with large chromo...

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Published in:Environmental microbiology Vol. 18; no. 10; pp. 3482 - 3493
Main Authors: Hocquet, Didier, Petitjean, Marie, Rohmer, Laurence, Valot, Benoît, Kulasekara, Hemantha D., Bedel, Elodie, Bertrand, Xavier, Plésiat, Patrick, Köhler, Thilo, Pantel, Alix, Jacobs, Michael A., Hoffman, Lucas R., Miller, Samuel I.
Format: Journal Article
Language:English
Published: England Blackwell Publishing Ltd 01-10-2016
Wiley Subscription Services, Inc
Society for Applied Microbiology and Wiley-Blackwell
Series:Ecophysiology of Pseudomonas
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Summary:Summary When bacterial lineages make the transition from free‐living to permanent association with hosts, they can undergo massive gene losses, for which the selective forces within host tissues are unknown. We identified here melanogenic clinical isolates of Pseudomonas aeruginosa with large chromosomal deletions (66 to 270 kbp) and characterized them to investigate how they were selected. When compared with their wild‐type parents, melanogenic mutants (i) exhibited a lower fitness in growth conditions found in human tissues, such as hyperosmolarity and presence of aminoglycoside antibiotics, (ii) narrowed their metabolic spectrum with a growth disadvantage with particular carbon sources, including aromatic amino acids and acyclic terpenes, suggesting a reduction of metabolic flexibility. Despite an impaired fitness in rich media, melanogenic mutants can inhibit their wild‐type parents and compete with them in coculture. Surprisingly, melanogenic mutants became highly resistant to two intraspecific toxins, the S‐pyocins AP41 and S1. Our results suggest that pyocins produced within a population of infecting P. aeruginosa may have selected for bacterial mutants that underwent massive gene losses and that were adapted to the life in diverse bacterial communities in the human host. Intraspecific interactions may therefore be an important factor driving the continuing evolution of pathogens during host infections.
Bibliography:istex:6FF0C7378F3FEC66CA4A6532874DA6C11AF8ADCC
ark:/67375/WNG-WC8SFQWK-9
ArticleID:EMI13336
ObjectType-Article-1
SourceType-Scholarly Journals-1
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PMCID: PMC5295658
ISSN:1462-2912
1462-2920
DOI:10.1111/1462-2920.13336