T6P/SnRK1信号途径在番茄花柄脱落中的作用及机制研究

Flower and fruit abscission is an important factor to affect the yield of fruit-vegetables. Abscission may occur as a response to carbohydrates starvation caused by environmental stress, such as low temperature, weak light. It has been shown that trehalose-6-phosphate (T6P) as an important signaling molecular involve in the regulation of plant growth and development in response to carbon availability. Several studies have speculated that T6P may participate in abscission induction together with hormones, while this need more researches. Our previous study has found that the transcriptional level of gene involved in T6P synthesis was higher in shading tomato pedicels than in control. In this work, the herbicide metamitron will be used to block photosynthesis and induce carbon starvation which will cause pedicel abscission in tomato. The T6P/SnRK1 signaling pathway and the abscission signals in response to carbon deficiency will be investigated from transcriptional level and metabolic level. We will explore the gene(s) in T6P/SnRK1 signaling pathway which show co-expression pattern(s) with genes related to abscission by bioinformatic methods. The VIGS approach were used to silence the gene(s) of T6P/SnRK1 signaling pathway which may regulate the expression of abscission signal, and uncover molecular mechanism of T6P/SnRK1 signaling on tomato pedicel abscission. To clarify this mechanism will be helpful to understand the abscission signal transduction system and provide theoretical basis for the increase of vegetable production.

光合同化物不足是造成落花落果的重要原因之一。研究表明，同化物供应不足时，植物中海藻糖-6-磷酸（T6P）作为重要的糖信号分子，可能与激素共同参与调控器官脱落，具体机制尚未阐明。我们前期研究发现，遮光诱导脱落的番茄花柄中T6P合成酶基因上调表达。本研究拟在此基础上通过外施光合抑制剂阻止番茄合成光合同化物，诱导番茄花柄脱落，分别从转录和代谢产物水平研究番茄中T6P介导的T6P/SnRK1信号途径，以及响应同化物供应不足的脱落信号途径；通过生物信息学技术挖掘T6P/SnRK1信号途径上调控脱落信号传导的关键基因，推测T6P/SnRK1信号途径在同化物供应不足诱导器官脱落中的作用；通过VIGS技术沉默T6P/SnRK1信号途径上的关键基因，阐明该途径在番茄花柄脱落中的作用机制。为深入研究植物脱落信号传导网络奠定基础，也为生产上通过栽培管理措施来调控植物器官脱落提供理论依据。

光合同化物不足是造成落花落果的重要原因之一，严重影响果菜类蔬菜产量，其具体机制尚未阐明。本研究通过遮光处理削弱番茄光合作用，降低同化物合成，诱导番茄花柄脱落，分别从转录和代谢产物水平探究了番茄中海藻糖-6-磷酸（T6P）合成代谢通路，T6P/SnRK1信号通路，以及激素信号通路在花器官脱落中的作用机制；通过生物信息学方法挖掘T6P合成代谢通路上调控T6P含量变化的关键基因，并通过VIGS技术沉默关键基因，分析T6P在同化物供应不足诱导器官脱落中的作用机制。结果表明：弱光下，番茄植株的光合作用受到抑制，光合产物积累减少，T6P作为感知植物碳源可用性的重要信号分子，其在脱落的花中的含量显著降低，而受T6P调控的关键激酶SnRK1变得活跃，受该酶调控的marker基因表达增强，这表明T6P及其信号转导通路参与了花器官脱落的过程。弱光诱导脱落的花器官中淀粉含量显著降低，通过VIGS技术沉默SlTPS1和SlTPP1的番茄植株中也发现淀粉降解过程受到T6P含量变化的调控，因此，我们推测番茄花器官脱落与T6P调控淀粉降解过程有关。此外，在脱落的花中发现激素ABA，乙烯含量显著升高，而生长素IAA含量显著降低，参与相应激素信号转导的基因表达也发生了显著变化，这表明上述激素参与了番茄花器官脱落过程。综上所述，我们提出了弱光诱导番茄花脱落的假设模型：在弱光诱导脱落的番茄花中，T6P作为“C”源供应不足的信号，调控了花中淀粉的降解过程。当栽培环境持续弱光时，番茄花中的淀粉不断降解，最终将导致花中淀粉“耗尽”；另一方面，弱光时，ABA，乙烯和生长素等激素转导途径启动，参与调控番茄花器官的脱落。本项目为深入研究植物脱落信号传导网络奠定基础，也为生产上通过栽培管理措施来调控植物器官脱落提供理论依据。