NPR1与EIN3拮抗介导高温诱导叶片衰老褪绿的分子机理研究

营固着生活方式的植物为保障新生器官的营养供给演化出了特有的营养运筹策略，即通过启动次要器官的递进式、模块化衰老来进行营养的动员与再分配。叶片是主要的模块化器官，成熟后营同化作用，启动衰老后则是主要的营养源器官，作物种子蛋白的合成主要依赖于衰老叶片转运出来的氨基酸。多种因素可以诱导叶片启动衰老，但是高温胁迫如何启动这一过程尚缺少探索。前期分析发现，乙烯信号组分EIN3正调控这一过程，而水杨酸信号组分NPR1则负调控这一个过程。已经鉴别出高温胁迫下EIN3的上游负调控节点SPL1/12，并发现EIN3能够自激活转录；还鉴别出了EIN3的互作蛋白XBAT35.1，以及NPR1的转录调控因子WRKY46/6。拟继续以EIN3和NPR1为切入点，系统地鉴别它们的上游调控因子和互作因子，重点分析水杨酸和乙烯信号在高温胁迫下的交互作用机制，藉此揭示高温胁迫启动叶片衰老的分子机制。

To maximize the supply of nutrients to rapidly growing/developing organs, sessile plants have evolved a characteristic strategy, i.e. to remobilize nutrients from less important modular organs by initiating their senescence. Leaves are major modular organs of plants, especially annual and biennial plants, acting as assimilation organs after fully mature, and sooner or later becoming source organs upon the initiation of senescence. Diverse factors could induce the initiation of leaf senescence, but how high temperature initiates leaf senescence remains elusive. Our preliminary analyses showed that EIN3, the key downstream component of ethylene signaling, positively regulates high temperature-triggered leaf senescence, whereas NPR1, the core signaling component/receptor of salicylic acid (SA), negatively regulates the process. We have also identified SPL1/12 as negative transcriptional regulators of EIN3 and WRKY46/6 as the positive transcriptional factors of NPR1, revealed a possible self-activation activity of EIN3 to its encoding gene EIN3, and characterized XBAT35.1 as an interaction protein of EIN3. In this project, we would like to identify additional upstream regulators of both EIN3 and NPR1 genes and their interaction proteins, and particularly to analyze the cross-talk between ethylene signaling and SA signaling, with an aim of elucidating the molecular mechanism by which high temperature triggers leaf senescence in Arabidopsis.