Lignin composition and timing of cell wall lignification are involved in Brassica napus resistance to Sclerotinia sclerotiorum stem rot

Abstract

Sclerotinia stem rot (SSR) is an economically and globally significant disease in oilseed rape (Brassica napus L.) caused by the necrotrophic ascomycete Sclerotinia sclerotiorum. This study explored the role of cell wall reinforcement by lignin as a relevant factor for effective plant defence against attack of this pathogen. Expression of key genes in the phenylpropanoid pathway and the induced synthesis of lignin in infected stem tissues were investigated in a study comparing a susceptible (Loras) and a moderately resistant cultivar (Zhongyou 821, ZY821). Data revealed an earlier and more rapid defence activation in ZY821 through up-regulation of transcript levels of genes related to key steps in the phenylpropanoid pathway associated with enhanced lignin deposition in the resistant B. napus genotype. Expression level of BnCAD5, encoding a cinnamyl alcohol dehydrogenase, responsible for conversion of monolignol to lignin, was more rapidly up-regulated in ZY821 than Loras. The similar expression pattern of BnCAD5 and the gene BnF5H, encoding for the ferulate-5-hydroxylase which catalyses the synthesis of syringyl (S) lignin precursors, suggests that BnCAD5 is involved in the S lignin formation. Histological observations confirmed these results, showing an earlier increase of S lignin deposition in the infected resistant genotype. Deposition of guaiacyl (G) lignin was detected in both genotypes and is thus considered a component of basal, cultivar-independent defence response of B. napus to stem rot. The results indicate the importance of cell wall modification for quantitative stem rot resistance by responses in the phenylpropanoid metabolism generating distinct lignin types on different temporal scales.