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Pseudomonas aeruginosa modulates both Caenorhabditis elegans attraction and pathogenesis by regulating nitrogen assimilation. | LitMetric

AI Article Synopsis

  • Detecting chemical signals helps organisms find food and avoid dangers.
  • Research shows that the small RNA P11 in Pseudomonas aeruginosa plays a role in attracting C. elegans to bacteria by influencing ammonia production.
  • This study reveals how nitrogen assimilation by bacteria affects both their fitness and their interaction with hosts like C. elegans, highlighting the importance of this process for signaling between species.

Article Abstract

Detecting chemical signals is important for identifying food sources and avoiding harmful agents. Like many animals, C. elegans use olfaction to chemotax towards their main food source, bacteria. However, little is known about the bacterial compounds governing C. elegans attraction to bacteria and the physiological importance of these compounds to bacteria. Here, we address these questions by investigating the function of a small RNA, P11, in the pathogen, Pseudomonas aeruginosa, that was previously shown to mediate learned pathogen avoidance. We discovered that this RNA also affects the attraction of untrained C. elegans to P. aeruginosa and does so by controlling production of ammonia, a volatile odorant produced during nitrogen assimilation. We describe the complex regulation of P. aeruginosa nitrogen assimilation, which is mediated by a partner-switching mechanism involving environmental nitrates, sensor proteins, and P11. In addition to mediating C. elegans attraction, we demonstrate that nitrogen assimilation mutants perturb bacterial fitness and pathogenesis during C. elegans infection by P. aeruginosa. These studies define ammonia as a major mediator of trans-kingdom signaling, implicate nitrogen assimilation as important for both bacteria and host organisms, and highlight how a bacterial metabolic pathway can either benefit or harm a host in different contexts.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11387622PMC
http://dx.doi.org/10.1038/s41467-024-52227-3DOI Listing

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