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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 |
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Main Authors: | , , , , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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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. |
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ISSN: | 2399-3642 2399-3642 |
DOI: | 10.1038/s42003-024-06947-3 |