Abstract
To investigate the effects of temperature on Brassica napus (canola) resistance to Leptosphaeria maculans (LM) the causal agent of blackleg disease, metabolic profiles of LM infected resistant (R) and susceptible (S) canola cultivars at 21ºC and 28ºC were analyzed. Metabolites were detected in cotyledons of R and S plants at 48- and 120-hours post-inoculation with LM using UPLC-QTOF/MS. The mock-inoculated plants were used as controls. Some of the resistance-related specific pathways, included lipid metabolism, amino acid metabolism, carbohydrate metabolism, and aminoacyl-tRNA biosynthesis, were down-regulated in S cultivar but up-regulated in R cultivar at 21ºC. However, some of these pathways were down-regulated in R cultivar at 28°C. Amino acid metabolism, lipid metabolism, alkaloid biosynthesis, phenylpropanoid biosynthesis, and flavonoid biosynthesis were the pathways linked to combined heat and pathogen stresses. By using network analysis and enrichment analysis, these pathways were identified as important. The pathways of carotenoid biosynthesis, pyrimidine metabolism, and lysine biosynthesis were identified as unique mechanisms related to heat stress and may be associated to the breakdown of resistance to the pathogen. The increased susceptibility of R plants to 28°C results in the down-regulation of signal transduction pathway components and compromised signaling, particularly during the later stages of infection. Deactivating LM-specific signaling networks in R plants may result in compatible responses, potentially drop in signaling metabolites under combined stress, highlighting global temperature challenges.