赤霉素和生长素之间的信号互作是植物学领域的研究热点，但二者之间的作用机理还知之甚少。我们的研究已经揭示了蛋白磷酸酶TOPP4通过对DELLA蛋白的去磷酸化调控了GA信号通路。在此基础上，前期实验通过筛选topp4-1 突变体的抑制子，发现生长素液泡膜转运蛋白WAT1的突变可以恢复其GA缺陷表型，WAT1能改变TOPP4的亚细胞定位，二者共定位并在液泡膜上相互作用。项目拟以WAT1和TOPP4的遗传与分子互作为切入点，通过WAT1与GA生物合成及信号转导通路突变体的遗传关系，揭示WAT1在其中的功能，确定WAT1为GA信号通路下游的新组分；通过TOPP4和WAT1蛋白互作、WAT1蛋白去磷酸化分析、TOPP4酶活性检测等，确定WAT1是作为TOPP4的底物蛋白还是调节亚基来恢复topp4-1突变体表型的机理，阐明TOPP4在生长素信号通路中的作用，揭示GA与生长素信号通路互作的新的分子机理。

The cross talking between gibberellin and auxin signaling pathways is one of the hot topics in plant biology research, but their mechanism is still poorly understood. In our previous studies, we identified that the protein phosphatase TOPP4 regulates gibberellin signaling by dephosphorylating DELLA proteins. Based on these findings, we used topp4-1 mutant as background material to find out its suppressors by EMS mutagenesis. We found that topp4-1 wat1 double mutant can recover the gibberellin defect phenotypes of topp4-1 mutant. WAT1 encodes a vacuolar auxin transport facilitator. WAT1 protein specificly localizes to the vacuolar membrane of the cell. TOPP4 protein ubiquitously localizes to the cytoplasm, nucleus and plasma membrane. While co-expressing of the two proteins showed that WAT1 can change the subcellular localization of TOPP4 to the vacuolar membrane. And protein interaction assays showed that WAT1 can directly interact with TOPP4. The present project plans to take advantage of the genetic and molecular interaction between WAT1 and TOPP4 as the key to identify the possible function and position of WAT1 played in GA signaling and to further identify that WAT1 is a new factor in GA signaling by constructing double mutants with gibberellin biosynthesis and signal transduction mutants. The main goal is to reveal whether WAT1 is a substrate protein or a regulatory subunit of TOPP4 by dephosphorylation analysis and phosphatase activity assay based on the protein interaction. Through these experiments, we plan to find the mechanism of wat1 mutation restoring the phenotypes of topp4-1 mutant and the role of TOPP4 played in auxin signaling pathway. The project is expected to elucidate a new cross talking mechanism between gibberellin and auxin signaling pathways through WAT1 and TOPP4 proteins.