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Epigallocatechin‐3‐gallate functions as a physiological regulator by modulating the jasmonic acid pathway
Author(s) -
Hong Gaojie,
Wang Jie,
Hochstetter Danielle,
Gao Yuanyuan,
Xu Ping,
Wang Yuefei
Publication year - 2015
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/ppl.12256
Subject(s) - jasmonic acid , arabidopsis thaliana , botrytis cinerea , biology , arabidopsis , mutant , signal transduction , polyphenol , biochemistry , regulator , microbiology and biotechnology , botany , salicylic acid , gene , antioxidant
Flavonoids, a class of plant polyphenols derived from plant secondary metabolism, play important roles in plant development and have beneficial effects on human health. Epigallocatechin‐3‐gallate ( EGCG ) is the most abundant polyphenol, and its molecular and biochemical mechanism have been followed with interest. The shared signaling heritage or convergence of organisms has allowed us to extend this research into the model plant, Arabidopsis thaliana . Here, we showed that EGCG could promote jasmonic acid ( JA ) signaling in A. thaliana . EGCG not only inhibited seed germination but also elevated the resistance to necrotrophic Botrytis cinerea , partly by altering the relative strength of JA signaling. Accordingly, JA marker gene induction, seed germination inhibition and the increased resistance to B. cinerea were attenuated in the JA ‐insensitive coi1‐2 mutant. The coi1‐2 mutant was partially insensitive to the treatment of EGCG , further implicating the function of EGCG in JA signaling and/or perception. Our results indicate that EGCG , a member of the flavonoid class of polyphenols, affects signal processing in seed development and disease susceptibility via modulation of JA signaling.