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

被引:78
作者
Min, Dedong [1 ]
Li, Fujun [1 ]
Cui, Xixi [1 ]
Zhou, Jingxiang [1 ]
Li, Jiaozhuo [1 ]
Ai, Wen [1 ]
Shu, Pan [1 ]
Zhang, Xinhua [1 ,2 ]
Li, Xiaoan [1 ]
Meng, Demei [3 ]
Guo, Yanyin [1 ]
Li, Jian [2 ]
机构
[1] Shandong Univ Technol, Sch Agr Engn & Food Sci, Zibo 255049, Shandong, Peoples R China
[2] BTBU, Beijing Engn & Technol Res Ctr Food Addit, Beijing 100048, Peoples R China
[3] Tianjin Univ Sci & Technol, Coll Food Engn & Biotechnol, Minist Educ China, Key Lab Food Nutr & Safety, Tianjin 300457, Peoples R China
基金
中国国家自然科学基金;
关键词
MYC2 transcription factor; Methyl jasmonate; Tomato fruit; Disease resistance; DISEASE RESISTANCE; PENICILLIUM-EXPANSUM; BLIGHT RESISTANCE; DEFENSE RESPONSES; ALPHA-TOMATINE; SALICYLIC-ACID; BIOSYNTHESIS; PROTEIN; MYC2; JA;
D O I
10.1016/j.foodchem.2019.125901
中图分类号
O69 [应用化学];
学科分类号
081704 ;
摘要
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, beta-1,3-glucanase and chitinase activities, as well as alpha-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, SIPRs expression, alpha-tomatine, special phenolic acids and flavonoid compounds.
引用
收藏
页数:9
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