SlMYC2 are required for methyl jasmonate-induced tomato fruit resistance to Botrytis cinerea.

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ID: 70886
2019
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Abstract
The mechanism of SlMYC2, involved in methyl jasmonate (MJ)-induced tomato fruit resistance to pathogens, was investigated. The data indicated that MJ treatment enhanced the accumulation of total phenolics and flavonoids, as well as individual phenolic acids and flavonoids, which might be caused by the increased phenylalanine ammonia-lyase and polyphenol oxidase activities, induced pathogenesis-related gene (PR) expression, β-1,3-glucanase and chitinase activities, as well as α-tomatine, by inducing GLYCOALKALOID METABOLISM gene expression. These effects, induced by MJ, partly contributed to tomato fruit resistance to Botrytis cinerea. Nevertheless, the induction effects of MJ were almost counteracted by silence of SlMYC2, and the disease incidence and lesion diameter in MJ + SlMYC2-silenced fruit were higher than those in MJ-treated fruit. These observations are the first evidence that SlMYC2 plays vital roles in MJ-induced fruit resistance to Botrytis cinerea, possibly by regulating defence enzyme activities, SlPRs expression, α-tomatine, special phenolic acids and flavonoid compounds.
Reference Key
min2019slmyc2food Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Min, Dedong;Li, Fujun;Cui, Xixi;Zhou, Jingxiang;Li, Jiaozhuo;Ai, Wen;Shu, Pan;Zhang, Xinhua;Li, Xiaoan;Meng, Demei;Guo, Yanyin;Li, Jian;
Journal Food chemistry
Year 2019
DOI
S0308-8146(19)32039-4
URL
Keywords
disease resistance methyl jasmonate myc2 transcription factor tomato fruit

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