设施弱光导致番茄病害高发中糖转运蛋白STP的作用及其调控机制

In greenhouse cultivation, low light not only affects production and quality of agroecosystems, but also dampen plant inner defense, causing disease susceptibility and threatening food safety. However, knowledge of the effects of low light on diseases and underlying mechanism is much lacking. Based on our current finding that a sugar transport protein SlSTP2 play a pivotal role in mediating tomato susceptibility against pathogen under low light, we will construct and use series of SlSTP2 transgenic over-expression lines, CRISPR mutant lines and VIGS gene-silenced tomato lines to dissect the underlying mechanism for their response to two different types of popular plant pathogens (bacterial leaf speck disease P. syringae and fungal leaf mold C. fulvum) under control and low light. In details, the inactivation mechanism of STP in response to low light will be examined at both substrate level and transcripts regulation level through approaches of 14C isotope labeling technology, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation-qPCR (ChIP-qPCR). The functionary mechanism of SlSTP2 and its uncoupling with FLS2-BAK1 complex pathway and/or sugar signaling pathway in susceptibility against pathogens under low will be evaluated using coimmunoprecipitation (Co-IP), split-ubiquitin yeast two-hybrid, and bimolecular fluorescence complementation (BiFC) technologies. Meanwhile, the alleviatory effects of elevated CO2 which can potentially regulate STP will also be examined. These results will not only give insight into the role and the mechanism involved in sugar transporter protein STP-mediated disease susceptibility under low light, but also supply theoretical basis for enhancing the vegetables plant defense and safety in suboptimal light intensity conditions, and therefore is of fundamental significance for horticultural science and industry.

设施弱光不仅使作物产量品质下降，也会导致病害高发，威胁蔬菜产品安全，但弱光与作物抗病性关系远不清楚。项目拟在前期发现弱光下糖转运蛋白（SlSTP2）表达抑制，并导致番茄对病害敏感的基础上，以番茄SlSTP2过表达、CRISPR突变、基因沉默植株，以及叶斑病菌、叶霉病菌为材料，通过14C-己糖饲喂、EMSA和ChIP等技术解析弱光下SlSTP2在底物及转录水平上的钝化机理；利用Co-IP、酵母双杂、BiFC等鉴定SlSTP2与关键蛋白的互作及其对光强的响应，挖掘弱光下番茄SlSTP2介导的敏感性与FLS2-BAK1复合体途径、HXK糖信号途径的关系及内在机制。探讨具潜在STP调控活性的CO2加富对弱光下番茄抗病性的影响及机制。项目将阐明设施弱光导致番茄敏感性变化中糖转运蛋白STP的关键作用及其调控机制，有助于解决困扰园艺作物弱光下抗性下降导致的病害高发问题，为设施安全高效生产提供理论基础。

设施弱光不仅使作物产量品质下降，也会导致病害高发，威胁蔬菜产品的安全，但弱光与作物抗病性的关系远不清楚。项目以番茄为材料，围绕弱光环境如何影响糖代谢、糖信号途径调控作物抗病性等问题开展研究，明确了糖转运蛋白STP2与糖信号传导途径G蛋白β亚基互作，正调控番茄对细菌性叶斑病的抗性；发现番茄通过G蛋白感知并传导葡萄糖信号调控弱光下番茄对Pst DC3000的抗性；进一步研究发现CO2 加富能增加弱光下番茄的抗病性。项目加深了我们对于糖代谢/信号途径在弱光环境下植物抗病性中作用机理的理解，有助于解决困扰园艺作物弱光下抗性下降导致的病害高发问题，为设施安全高效生产提供理论基础。项目执行期间共培养博士后1名，博士研究生4名，硕士研究生2名。项目负责人以第一或通讯作者在 Plant Cell、New Phytologist等主流国际刊物上发表本项目的资助论文 13 篇，其中 IF5year 大于 5.0 的论文 8 篇。另本项目成果申报并获授权国家发明专利3 项。积极参加学术活动，在 5 个国内外学术会议上报道了本项目的研究成果。