磷脂酸（PA16:0-18:2）与乙烯信号元件CTR1协同调控桃果实冷害机制

冷害是园艺产品采后损耗严重的共性原因之一，膜脂重塑是冷害发生关键上游事件，磷脂酸再构是膜脂重塑核心。申请人前期研究发现，冷害关键磷脂酸（PA16:0-18:2）分子及其代谢基因皆负调控乙烯信号，且乙烯信号正调控果实抗冷，但PA如何介导乙烯信号调控冷害机制不明。申请人分析发现桃乙烯信号元件CTR1蛋白具有PA结合区域，故推测，PA16:0-18:2靶向CTR1负调控乙烯信号影响果实冷害。据此，本项目拟以冷敏型桃果实为试材，运用VIGS、脂质组、PA及其合成抑制剂外源处理等方法和手段，揭示PA对乙烯和冷害的作用规律；从自身磷酸化水平、与乙烯受体PpETR1的作用、体外结合和活性表征，三个方面系统解析PA对PpCTR1的调控机理；并利用外源乙烯处理进一步确证。项目成果可阐明“PA-CTR1”模块介导乙烯信号调控冷害机制，为控制冷害提供新思路。

Chilling injury (CI) is one of the most common causes of postharvest horticultural product losses, and membrane lipid remodeling is an important upstream event in which phosphatidic acid (PA) plays a key role. According to a previous study by the applicant, PA 16:0-18:2 was discovered to be closely associated to CI, and its metabolic gene negatively regulated ethylene signaling, resulting in peach fruit chilling tolerance. According to bioinformatics analysis, peach CTR1 has a PA binding region, suggesting that PA 16:0-18:2 targets CTR1 and negatively regulates ethylene signaling to modulate CI. To test this hypothesis, peaches with chilling sensitivity will be used in this project, along with a variety of methods and techniques such as VIGS, lipidomics, and exogenous treatments with the PA and its inhibitors, to uncover the essence of the PA's effects on ethylene and internal browning of CI; the mechanism by which the PA regulates PpCTR1 will be investigated in three aspects: PpCTR1 phosphorylation, PpCTR1-PpETR1 interaction, and PA effects on recombinant PpCTR1 protein. The findings of this project will aid in the understanding of the mechanism of peach fruit CI involved in ethylene signaling regulated by the 'PA-CTR1' module, as well as provide new insights into controlling horticultural products from CI.