Resistant responses of tomato fruit treated with exogenous methyl jasmonate to Botrytis cinerea infection

In this paper, we investigated the effect of exogenous methyl jasmonate (MeJA) on gray mould rot caused by Botrytis cinerea in tomato fruit and its mechanism related to reactive oxygen species (ROS) metabolism. The results indicated that MeJA at a concentration of 10 mM effectively inhibited lesion diameter of gray mould rot in tomato fruit. Resistant response of MeJA-treated tomato fruit to B. cinerea was attributed to an accumulation of H2O2, concomitant with enhanced Cu–Zn superoxide dismutase (Cu–Zn SOD) gene expression and decreased catalase (CAT) transcript level during the early stage of storage. However, MeJA treatment stimulated CAT and ascorbate peroxidase (APX) gene expression, enhanced ascorbate (ASC) and glutathione (GSH) content, being beneficial for scavenging excess ROS and alleviating oxidative damage of proteins. These results indicated that mechanisms involved in the induction of the fruit resistance to B. cinerea might be associated with elicitation of antioxidative reaction and prevention of protein carbonylation in fruit. In addition, MeJA negatively affected plasma membrane integrity of B. cinerea spores and showed direct antimicrobial activity in vitro, suggesting MeJA has direct fungitoxic property against the pathogen.

► We investigated the effect of methyl jasmonate (MeJA) on oxidative defense to Botrytis cinerea in tomato fruit.
► MeJA treatment can increase antioxidant capacity of fruit to scavenge excess ROS.
► We used new biochemical markers in tomato fruit to confirm that MeJA alleviated pathogen-induced oxidative damage.