转录因子FHY3/FAR1在远红光诱导番茄耐低温性中的作用机制

Low temperature often limits the growth and development of vegetables, so it is of great significance to explore the regulation mechanisms and protecting technologies of vegetables during cold stress. Recently, we have found that far-red light (FR) could increase the chilling tolerance of tomato plants via its primary photoreceptor phytochrome A (phyA). Previous reports showed that the transposase-derived transcription factors FAR-RED ELONGATED HYPOCOTYL3 (FHY3) and its homolog FARRED-IMPAIRED RESPONSE1 (FAR1) act in phyA signaling, and promote inositol biosynthesis in Arabidopsis, but whether FHY3/FAR1 could regulate inositol during FR induced chilling tolerance of tomato and its regulation mechanism remain largely unclear. Based on the found that genes expression of FHY3 and FAR1 were induced by FR under cold stress, in this project, we will study the role of FHY3/FAR1 in FR light-induced chilling tolerance in tomato by silencing and overexpressing the FHY3/FAR1 gene. Meanwhile, we will identify the critical downstream target genes of FHY3/FAR1 involved in inositol biosynthesis and dissect their roles in light quality-mediated chilling tolerance via transcriptomic data analysis and virus-induced gene silencing (VIGS), respectively. To further study the function of FHY3/FAR1, its transcriptional activation activity will be identified by yeast one-hybrid assay. In addition, we will analyze the interactions of FHY3/FAR1 transcription factor and its downstream target genes through EMSA, ChIP-qPCR and dual-luciferase assays. The functions and molecular mechanisms of FHY3/FAR1 regulation of inositol in FR light-induced chilling tolerance of tomato will be established from this research project, which will found theoretical basis for improving the chilling tolerance of vegetables via regulation of light-quality signals.

设施蔬菜低温生育障碍经常发生，探究其发生机理及防控技术意义重大。申请者近年发现远红光（FR）可通过光受体phyA提高番茄的耐低温性，且有研究表明：转录因子FHY3/FAR1参与phyA的信号转导，并诱导拟南芥肌醇的积累，但FHY3/FAR1是否通过调节肌醇参与FR诱导番茄耐低温性过程及其调控机制尚不清楚。因此，本项目在明确番茄FHY3/FAR1受低温及FR调控的基础上，构建其基因敲除及过表达植株，探究其在FR诱导番茄耐低温中的作用；利用转录组测序和VIGS技术，挖掘和验证受FHY3/FAR1调控的肌醇合成基因及其功能；通过酵母单杂交技术，分析FHY3/FAR1的转录激活活性；利用EMSA、ChIP-qPCR等技术，探索FHY3/FAR1与筛选到的肌醇合成基因间的互作机制。本项目旨在揭示FHY3/FAR1在FR诱导番茄耐低温性中的作用及调控机制，为利用光质诱导喜温蔬菜的耐低温性提供理论依据。

设施蔬菜低温生育障碍经常发生，探究其发生机理及防控技术意义重大，而光信号与温度信号经常耦合在一起调控植物的生长发育及抗逆性，因此探究光信号和温度信号的交叉互作机制有重要研究意义。本项目研究了光质信号调控番茄耐低温性的生理与分子机制。1）我们研究发现，低温下，远红光可以诱导番茄的耐低温性，低比例的红光/远红光能够显著诱导光信号转录因子SlFHY3的表达，而SlFHY3正调控番茄的耐低温性，揭示了番茄光信号因子SlFHY3低温下诱导番茄体内肌醇积累进而提高番茄耐低温性的作用机制。2）研究了远红光诱导番茄耐低温性中肌醇的调控作用，揭示了低温胁迫下番茄肌醇1-磷酸合酶基因SlMIPS3通过促进肌醇合成进而提高番茄耐低温性的作用机制。3）利用遗传学和生理生化等研究方法，明确了番茄肌醇1-磷酸合酶基因SlMIPS3在SlFHY3下游发挥作用。本项目阐明了远红光信号通过激活光信号转录因子SlFHY3，从而促进肌醇1-磷酸合酶基因SlMIPS3的表达，诱导番茄体内肌醇的积累，进而提高番茄耐低温性的作用机制。本项目为设施蔬菜生产中利用LED光谱技术防控低温逆境障碍提供了理论基础和实践指导。相关研究结果在《New Phytologist》《Plant Biotechnology Journal》《Frontiers in Plant Science》《园艺学报》《中国农业科学》等国内外重要学术期刊上发表标注论文6篇，SCI累计影响因子33.194，申请国家发明专利1项，培养中青年学术带头人（优青）1人，做学术会议报告2次。