Differential expression of antimicrobial metabolites, phenylpropanoid and phytohormone metabolic pathway genes determines resistance or susceptibility to Ascochyta rabiei in chickpea

Abstract

AbstractBlight caused by Ascochyta rabiei is a major constraint in the productivity of chickpea (Cicer arietinum). The mechanisms governing resistance/susceptibility to blight in chickpea are poorly understood. We used a blight‐resistant (HC1) and a blight‐susceptible (GPF2) genotype of chickpea and genes of pathogenesis‐related proteins (PRPs), phenylpropanoid pathway metabolites, abscisic acid (ABA), gibberellic acid (GA) and jasmonic acid (JA) to understand the role of these in A. rabiei resistance/susceptibility. The JA, ABA and GA biosynthesis genes of chickpea were retrieved, characterized and gene‐specific primers were used for transcriptional studies. Gene expression revealed that chickpea activated its defences rather quickly and well before initiation of spore germination. In resistant HC1, the majority of the JA, GA and phenylpropanoid pathway genes had peak maxima at 2 h post‐inoculation (hpi) whereas PRPs/defence genes had peak maxima at 24/36 hpi implying that defence to A. rabiei in chickpea is composed of a two‐tier system separated by time: immediately after spore attachment and at or just prior to host penetration. Unlike HC1, susceptible GPF2 was late in activation of defence responses or did not activate them. Another striking difference between HC1 and GPF2 was up‐regulation of ABA biosynthesis genes in inoculated GPF2 and down‐regulation in HC1. This study revealed that phenylpropanoids, PRPs, JA, 8‐(1R,2R)‐3‐oxo‐2‐(Z)‐pent‐2‐enyl cyclopentyl octanoate, (15Z)‐12‐oxophyto‐10,15‐dienoic acid and methyl‐jasmonate govern resistance to A. rabiei in chickpea whereas ABA governs susceptibility.