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Secondary metabolites influence Arabidopsis/ Botrytis interactions: variation in host production and pathogen sensitivity
Author(s) -
Kliebenstein Daniel J.,
Rowe Heather C.,
Denby Katherine J.
Publication year - 2005
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2005.02508.x
Subject(s) - arabidopsis , botrytis , botrytis cinerea , pathogen , biology , virulence , arabidopsis thaliana , secondary metabolite , phytoalexin , microbiology and biotechnology , metabolite , human pathogen , mutant , botany , genetics , biochemistry , gene , resveratrol
Summary Numerous studies have suggested that plant/pathogen interactions are partially mediated via plant secondary metabolite production and corresponding pathogen tolerance. However, there are inconsistent reports on the ability of particular compounds to provide resistance to a pathogen. Most of these studies have focused on individual isolates of a given pathogen, suggesting that pathogens vary in their sensitivity to plant‐produced toxins. We tested variability in virulence among pathogen isolates, and the impact on this by plant production of, and pathogen tolerance to, secondary metabolites. Botrytis cinerea isolates showed differing sensitivity to purified camalexin, and camalexin‐sensitive isolates produced larger lesions on camalexin‐deficient Arabidopsis genotypes than on the wild type. In contrast, the camalexin‐insensitive isolate produced lesions of similar size on wild‐type and camalexin‐deficient Arabidopsis. Additional analysis with Arabidopsis secondary metabolite biosynthetic mutants suggests that Botrytis also has variable sensitivity to phenylpropanoids and glucosinolates. Furthermore, Botrytis infection generates a gradient of secondary metabolite responses emanating from the developing lesion, with the Botrytis isolate used determining the accumulation pattern. Collectively, our results indicate that Arabidopsis/ Botrytis interactions are influenced at the metabolic level by variations in toxin production in the host and sensitivity in the pathogen.