以番茄为模式解析系统素和茉莉酸介导的植物防御信号通路

In tomato, the peptide signal systemin and the plant hormone jasmonate regulate plant defense to mechanical wounding, insect attack and pathogen infection through a common signaling pathway. Therefore, the systemin/jasmonate signaling pathway of tomato provides a unique model system to investigate the mechanism by which peptide and hormone signals coordinate plant defense. In this application, we propose to build up our previous success in using a forward genetic approach to identify tomato mutants that suppress system/jasmonate-regulated plant defense. The specific aims are: 1) to clone the SPR1 gene and elucidate its proposed action mechanism in systemin perception and in integrating the systemin action into the downstream jasmonate signaling pathway; 2) to elucidate how SPR5, which encodes the MED25 subunit of the Mediator transcriptional co-activator complex, interacts with the transcription factor SAP1 to activate the systemin/jasmonate signaling pathway; 3) to elucidate how MED15, another subunit of Mediator, interacts with the transcription factor SAP2 to attenuate the systemin/jasmonate signaling pathway. 4) to elucidate how SPR7, which encodes an importin-ß (IMPß), regulates the antagonistic interaction between systemin/jasmonate-signaled plant defense and salicylic acid-signaled plant defense. Results obtained from these studies promise to provide insight into the mechanisms by which the peptide systemin integrates its action with that of jasmonate, systemin/jasmonate activates and attenuates plant defense, as well as systemin/jasmonate-regulated plant defense inhibits salicylic acid-regulated plant defense.

在番茄中，多肽信号分子系统素和经典激素茉莉酸通过一条共同的信号通路调控植物防御。本项目将从分析系统素信号通路的抑制子spr1, spr5和spr7入手解析系统素-茉莉酸介导的植物防御。我们将克隆SPR1基因并阐明其整合系统素信号和茉莉酸信号的机理。SPR5编码转录中介体Mediator的亚基MED25。我们将揭示MED25与转录因子SAP1互作正向调控（激活）系统素-茉莉酸途径的机理；我们还将揭示Mediator的另一个亚基MED15与转录因子SAP2互作负向调控（消减）系统素-茉莉酸途径的机理。SPR7编码一个Importin-ß 蛋白，我们将阐明SPR7与转录辅助因子SIP1互作正向调控系统素-茉莉酸途径而负向调控水杨酸途径的分子机理。总之，本项目将从系统素信号与茉莉酸信号的整合、茉莉酸信号途径的“激活”与“消减”、茉莉酸与水杨酸的拮抗等方面阐明系统素-茉莉酸调控植物防御的分子机理。

在番茄中，多肽信号分子系统素和经典激素茉莉酸通过一条共同的信号通路调控植物防御。本项目从分析系统素信号通路的抑制子spr1、spr5和spr7入手解析系统素-茉莉酸介导的植物防御。. 我们证明SPR1编码系统素高亲和力受体SYR1，而其同源蛋白SYR2为系统素低亲和力受体。进一步研究发现较低浓度的系统素即可促进SYR1与共受体互作形成受体复合物，进而激活系统素-茉莉酸信号通路；随着系统素浓度的升高，SYR2与SYR1竞争结合共受体，从而消减系统素-茉莉酸信号通路。有趣的是，SYR2和系统素前体基因PROSYSTEMIN在植物受伤后受茉莉酸途径核心转录因子MYC2的诱导表达，而SYR1的表达水平则几乎不变。这样SYR1和SYR2形成负反馈通路将系统素-茉莉酸信号通路的激活和消减整合为一个极为精密的调控过程。. 我们发现转录中介体亚基SPR5/MED25在茉莉酸信号途径转录调控的各个层面都发挥重要作用。我们证明：1）MED25招募转录共激活子LUH，放大MYC2-MED25功能复合体的转录输出；2）MED25招募剪切因子PRP39a/40a，精确调控抑制子基因JAZ的可变剪切，从而精准控制茉莉酸信号的激活强度；3）MYC2-MED25靶向激活负调控因子MTB，从而与之形成负反馈回路，适时终止茉莉酸信号；4）MED25还通过介导增强子与启动子之间染色质环的形成而差异性地控制MYC2自身的表达，从而实现茉莉酸信号在激活和终止之间的灵活切换。. 我们还揭示了SPR7/IMPß介导的SIP1入核差异性地调控茉莉酸途径和水杨酸途径的分子机理。我们发现SPR7介导SIP1入核通过形成SPR7-SIP1-MYC2-MED25功能复合体，正向调控茉莉酸响应基因表达；另一方面，SPR7介导SIP1入核形成SPR7-SIP1-TGA功能复合体，负向调控水杨酸响应基因表达。. 综上所述，我们通过对spr1、spr5和spr7的研究，从系统素信号与茉莉酸信号的整合、茉莉酸信号途径的“激活”与“消减”、茉莉酸与水杨酸的拮抗等方面系统阐明了系统素-茉莉酸调控植物防御的分子机理。