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Cyclo(Pro-Tyr) elicits conserved cellular damage in fungi by targeting the [H+]ATPase Pma1 in plasma membrane domains

Bioactive metabolites play a crucial role in shaping interactions among diverse organisms. In this study, we identified cyclo(Pro-Tyr), a metabolite produced by Bacillus velezensis , as a potent inhibitor of Botrytis cinerea and Caenorhabditis elegans , two potential cohabitant eukaryotic organisms....

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Published in:Communications biology 2024-10, Vol.7 (1), p.1253-20, Article 1253
Main Authors: Vela-Corcia, D., Hierrezuelo, J., Pérez-Lorente, A. I., Stincone, P., Pakkir Shah, A. K., Grélard, A., Zi-Long, Y., de Vicente, A., Pérez García, A., Bai, L., Loquet, A., Petras, D., Romero, D.
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Language:English
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Summary:Bioactive metabolites play a crucial role in shaping interactions among diverse organisms. In this study, we identified cyclo(Pro-Tyr), a metabolite produced by Bacillus velezensis , as a potent inhibitor of Botrytis cinerea and Caenorhabditis elegans , two potential cohabitant eukaryotic organisms. Based on our investigation, cyclo(Pro-Tyr) disrupts plasma membrane polarization, induces oxidative stress and increases membrane fluidity, which compromises fungal membrane integrity. These cytological and physiological changes induced by cyclo(Pro-Tyr) may be triggered by the destabilization of membrane microdomains containing the [H + ]ATPase Pma1. In response to cyclo(Pro-Tyr) stress, fungal cells activate a transcriptomic and metabolomic response, which primarily involves lipid metabolism and Reactive Oxygen Species (ROS) detoxification, to mitigate membrane damage. This similar response occurs in the nematode C. elegans , indicating that cyclo(Pro-Tyr) targets eukaryotic cellular membranes. Cyclo(Pro-Tyr), a metabolite from Bacillus velezensis , inhibits Botrytis cinerea and Caenorhabditis elegans by disrupting membrane polarization, inducing oxidative stress, and increasing membrane fluidity. These effects trigger lipid metabolism and ROS detoxification, targeting eukaryotic membranes.
ISSN:2399-3642
2399-3642
DOI:10.1038/s42003-024-06947-3