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Resveratrol acts as a natural profungicide and induces self‐intoxication by a specific laccase
Author(s) -
Schouten Alexander,
Wagemakers Lia,
Stefanato Francesca L.,
Kaaij Rachel M. van der,
Kan Jan A. L. van
Publication year - 2002
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2002.02801.x
Subject(s) - phytoalexin , resveratrol , botrytis cinerea , laccase , biology , mutant , secondary metabolite , gene , microbiology and biotechnology , virulence , fungus , botrytis , wild type , metabolite , biochemistry , botany , enzyme
Summary The grapevine ( Vitis ) secondary metabolite resveratrol is considered a phytoalexin, which protects the plant from Botrytis cinerea infection. Laccase activity displayed by the fungus is assumed to detoxify resveratrol and to facilitate colonization of grape. We initiated a functional molecular genetic analysis of B. cinerea laccases by characterizing laccase genes and evaluating the phenotype of targeted gene replacement mutants. Two different laccase genes from B. cinerea were characterized, Bclcc 1 and Bclcc 2. Only Bclcc2 was strongly expressed in liquid cultures in the presence of either resveratrol or tannins. This suggested that Bclcc 2, but not Bclcc 1, plays an active role in the oxidation of both resveratrol and tannins. Gene replacement mutants in the Bclcc 1 and Bclcc 2 gene were made to perform a functional analysis. Only Bclcc 2 replacement mutants were incapable of converting both resveratrol and tannins. When grown on resveratrol, both the wild type and the Bclcc 1 replacement mutant showed inhibited growth, whereas Bclcc 2 replacement mutants were unaffected. Thus, contrary to the current theory, BcLCC2 does not detoxify resveratrol but, rather, converts it into compounds that are more toxic for the fungus itself. The Bclcc 2 gene was expressed during infection of B. cinerea on a resveratrol‐producing host plant, but Bclcc 2 replacement mutants were as virulent as the wild‐type strain on various hosts. The activation of a plant secondary metabolite by a pathogen introduces a new dimension to plant–pathogen interactions and the phytoalexin concept.