基于iTRAQ技术研究采后1-甲基环丙烯和乙烯利处理对茭白线粒体蛋白质组变化的影响

Effect of 1-Methyleyelopropene and Ethylene on Mitochondrial Proteome Changes in Postharvest Zizania latifolia Analyzed Using iTRAQ Labeling Technique

In order to explore the molecular mechanism of postharvest senescence of Zizania latifolia, the effect of 1-methyleyelopropene (1-MCP) and ethylene (ET) treatments on mitochondrial proteome changes in postharvest Z. latifolia after storage at 25 ℃ for 0 (control), 3 and 6 days were investigated by using isobaric tags for relative and absolute quantification (iTRAQ) labeling. The results showed that a total of 1 908 proteins were identified with at least two peptides, of which 315 proteins showed an 2.0-fold change in their relative quantitation in the untreated, ET-treated, 1-MCPtreated groups at day 3 and 6 of storage as compared to their counterparts at day 0, with statistically significant differences being observed between results from replicate experiments (P < 0.05). A bioinformatics analysis of these differentially expressed proteins revealed that metabolic pathways, the biosynthesis of secondary metabolites, the biosynthesis and metabolism of amino acids, nucleotide metabolism, and the metabolic pathways of nucleobase-containing small molecules were related to postharvest senescence of Z. latifolia and that the citrate cycle, oxidative phosphorylation (OXPHOS), the pentose phosphate pathway (PPP), C5-branched dibasic acid metabolism and amino acid metabolism may play critical roles in postharvest senescence of Z. latifolia. Based on their biological functions, postharvest senescence of Z. latifolia may be closely associated with accelerated carbohydrate hydrolysis as well as strengthened PPP and weakened glycolysis and OXPHOS, leading to reduced energy supply and aggravated oxidative damage and consequently activating Ca2+/MAPKs, cytochrome c and jasmonate signaling pathways to cause primary metabolic disturbance and an increase in the accumulation of secondary metabolites such as lignin and consequently induce cell apoptosis or necrosis and finally accelerate senescence.