Microbiome manipulation by a soil-borne fungal plant pathogen using effector proteins

During colonization of their hosts, pathogens secrete effector proteins to promote disease development through various mechanisms. Increasing evidence shows that the host microbiome plays a crucial role in health, and that hosts actively shape their microbiomes to suppress disease. We proposed that...

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Veröffentlicht in:Nature plants 2020-11, Vol.6 (11), p.1365-1374
Hauptverfasser: Snelders, Nick C., Rovenich, Hanna, Petti, Gabriella C., Rocafort, Mercedes, van den Berg, Grardy C. M., Vorholt, Julia A., Mesters, Jeroen R., Seidl, Michael F., Nijland, Reindert, Thomma, Bart P. H. J.
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Sprache:eng
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Zusammenfassung:During colonization of their hosts, pathogens secrete effector proteins to promote disease development through various mechanisms. Increasing evidence shows that the host microbiome plays a crucial role in health, and that hosts actively shape their microbiomes to suppress disease. We proposed that pathogens evolved to manipulate host microbiomes to their advantage in turn. Here, we show that the previously identified virulence effector VdAve1, secreted by the fungal plant pathogen Verticillium dahliae , displays antimicrobial activity and facilitates colonization of tomato and cotton through the manipulation of their microbiomes by suppressing antagonistic bacteria. Moreover, we show that VdAve1, and also the newly identified antimicrobial effector VdAMP2, are exploited for microbiome manipulation in the soil environment, where the fungus resides in absence of a host. In conclusion, we demonstrate that a fungal plant pathogen uses effector proteins to modulate microbiome compositions inside and outside the host, and propose that pathogen effector catalogues represent an untapped resource for new antibiotics. A secreted protein effector from the fungal pathogen Verticillium dahliae has bactericidal properties. It allows the pathogen to modify the root microbiome in tomato and cotton, specifically eliminating plant-protective bacteria, to increase its own virulence.
ISSN:2055-0278
2055-0278
DOI:10.1038/s41477-020-00799-5