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

• Methyl jasmonate (MJ) induced SlMYC2 expression and fruit resistance to B. cinerea. • MJ induced GLYCOALKALOID METABOLISM gene expressions and α-tomatine content. • MJ induced SPRs expression, total and special phenolic acids and flavonoid contents. • The silence of SlMYC2 counteracted the induced effects of MJ on tomato fruit. • SlMYC2 is involved in MJ-induced resistance to B. cinerea in tomato fruit. 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. [ABSTRACT FROM AUTHOR]