Role of methyl jasmonate and salicylic acid in kiwifruit plants further subjected to Psa infection: biochemical and genetic responses

Abstract

The use of plant elicitors for controlling Pseudomonas syringae pv. actinidiae (Psa), the etiological agent of the kiwifruit bacterial canker (KBC), has been analysed in the past and, while salicylic acid (SA) seems to decrease disease susceptibility, methyl jasmonate (MJ) shows an opposite effect. However, the metabolic and genomic responses of Psa-infected plants following elicitation with these two compounds, as compared with non-elicited Psa-inoculated plants, are poorly understood, being the focus of this study. Micropropagated A. chinensis ‘Hayward’ plants were elicited with MJ or SA, and further inoculated with Psa. Fifteen days post-inoculation, Psa population in MJ-treated plants was increased by 7.4-fold, whereas SA elicitation led to decreased Psa colonization (0.5-fold), as compared with non-elicited inoculated plants. Additionally, elicitation with MJ or SA generally decreased polyphenols and lignin concentrations (by at least 20%) and increased total proteins (by at least 50%). MJ led to the upregulation of SOD, involved in plant antioxidant system, and reporter genes for the jasmonic acid (JA) (JIH and LOX1), abscisic acid (SnRK), SA (ICS1), and ethylene (ACAS1, ETR1 and SAM) pathways. Moreover, it increased ABA (40%) and decreased carotenoids (30%) concentrations. Contrastingly, comparing with non-elicited Psa-inoculated plants, SA application resulted in the downregulation of antioxidant system-related genes (SOD and APX) and of reporter genes for ethylene (ETR1) and JA (JIH and ETR1). This study contributes to the understanding of potential mechanisms involved in kiwifruit plant defences against Psa, highlighting the role of the JA, ABA and ethylene in plant susceptibility to the pathogen.