维生素C是调控植物生长发育和逆境胁迫应答的重要因子，也是植物必需的抗氧化剂，剖析维生素C生物合成调控的分子机理对开展作物品质和耐逆性遗传改良具有重要的理论和现实意义。我们前期研究发现，植物激素脱落酸介导其信号分子ABI4抑制了维生素C的生物合成，导致活性氧产生，进而抑制拟南芥幼苗生长；进一步分析表明，脱落酸处理转录抑制了维生素C合成基因的表达，且ABI4可以与维生素C生物合成基因VTC2启动子元件互作，表明ABI4可能是调控维生素C生物合成基因表达的重要因子。本研究拟在以上研究基础上，利用abi4 vtc2双突变体分析ABI4与VTC2的遗传调控关系；通过鉴定ABI4与VTC2基因启动子顺式作用元件互作的关键氨基酸及核心元件位点，剖析ABI4转录调控VTC2基因表达的生化基础；进一步结合ABI4相关突变体材料进行转录表达谱分析，鉴定并阐明ABI4转录调控维生素C生物合成基因表达的分子基础。

Increasing investigations reveal that vitamin C is a pivotal antioxidant essential for plant responses to multiple stresses and plant growth development. Unraveling the underlying regulatory mechanisms of vitamin C biosynthesis has become one of the important aspects in plant physiology, which will provide guidance for genetic improvement of crop quality and resistance to environmental stresses. Previous researches indicate that abscisic acid (ABA), a significant phytohormone in plant stress responses, plays an important role in the regulation of plant growth and development. Especially, we previously found that ABI4, an AP2/ERF transcription factor in ABA signaling pathway, is the key regulator in ABA-inhibited seedling growth, through enhancing the production of reactive oxygen species (ROS), but reducing the biosynthesis of vitamin C. Since vitamin C is an important antioxidant to scavenge ROS, we then evidenced that vitamin C could restore ABA-inhibited seedlings growth, through reducing ROS generation. Thus our previous results establish that ABA mediating ABI4 inhibits vitamin C biosynthesis, resulting in the promotion of the ROS generation and inhibition of seedling growth. Analysis of transcriptome expression profiling and qPCR analysis showed that ABA mediating ABI4 inhibited the expression of VTC2, which encodes a key enzyme of vitamin C biosynthesis. Chromatin immune-precipitation assays revealed that ABI4 could directly bind to the promoter area of VTC2. Based on the above studies, we will further conduct the following investigations in the proposed project. Firstly, we will analyze the genetic regulatory basis between ABI4 and VTC2 using abi4 vtc2 double mutant. And then we will verify the interaction domains of ABI4 and the key cis-elements in VTC2 promoter, to elucidate the molecular mechanism of transcriptional repression of ABI4 in vitamin C biosynthesis. Next we will unravel the molecular basis of ABI4-involved in the regulation of vitamin C biosynthesis in Arabidopsis, through transcriptome sequencing with ABI4 loss-of-function mutants and overexpression transgenic lines.