P-Coumaric acid induces jasmonic acid-mediated phenolic accumulation and resistance to black rot disease in Brassica napus

Abstract

To investigate p-coumaric acid (pCA)-induced plant resistance, the regulation of jasmonic acid (JA)-mediated phenylpropanoid biosynthesis pathway was assessed in response to pre-treatment with pCA or an inhibitor of 4-coumarate–CoA ligase (4CL), 3,4-(methylenedioxy) cinnamic acid (MDCA), in Brassica napus cultivar (cv. Mosa) following Xanthomonas campestris pv. campestris (Xcc) inoculation. At seven days post inoculation with Xcc, necrotic lesions decreased in response to pCA pre-treatment. JA content and expression of signaling genes (COI1 and PDF1.2) were enhanced in pCA-pre-treated plants, along with an increase in the MYB transcriptional factor, production of anthocyanin pigment 1 (PAP1), which regulates phenylpropanoid biosynthesis in Xcc-inoculated plants. Following Xcc inoculation, the accumulation of epigallocatechin and epigallocatechin gallate was increased in soluble forms; however, induced accumulation of pCA, ferulic acid, and sinapic acid was observed in both soluble and cell wall-bound forms in response to pCA pre-treatment, whereas this decreased in control or MDCA pre-treated plants. The expression of phenylpropanoid biosynthesis-related genes was upregulated in plants pre-treated with pCA, whereas it decreased or did not change in control and MDCA pre-treated plants, following Xcc inoculation. These results indicate that treatment with pCA primed the JA-signaling mediated induction of phenylpropanoid biosynthesis to provoke disease resistance in B. napus to Xcc.