小麦TaGBF1-TaCKB4通路协调蓝光和盐胁迫应答信号交互的分子机制研究

The environmental stimuli orchestrate plant growth and crop production via cross-talk. Salt stress and light are two crucial environmental stimuli that negatively and positively affect plant growth, however they cross-talk and synergetically modulate the growth has not been addressed. Our group bred a wheat introgression cultivar SR3, and it exhibits superior salt tolerance at germination stage, and weaker photomorphogenesis capacity in comparison with the parent wheat JN177. The applicant previously identified a transcriptional repressor TaGBF1 (Plant J, 2015), the first component participating in the response to light and salt; its overexpression promoted blue light-mediated photomorphogenesis, and reduced salt tolerance via ABI5, the crucial factor of ABA signaling, while its RNAi showed an opposite effect (phenocopy SR3’s traits). However, the mechanism of TaGBF1 orchestrating the two processes is unclear. We further isolated a TaGBF1 target gene TaCKB4, who inhibited blue light-mediated photomorphogenesis but reduced salt tolerance; TaCKB4 interacted with HY5, the crucial factor of light-mediated photomorphogenesis signaling. In this project, we propose to elucidate how TaGBF1-TaCKB4 modulate photomorphogenesis via HY5, and decrease salt tolerance via ABI5. The perspective outcome will help us understand the mechanism of cross-talk between light and salt stress, and provide candidate genes for wheat (crop) molecular breeding.

不同环境因子通过交叉互作，协同调控植物生长发育和作物产量。盐胁迫和光分别抑制和促进生长发育，但其响应信号交叉和协同调控机制尚未报道。本课题组培育的小麦渐渗系耐盐品种SR3与亲本相比，萌发期耐盐性强，光形态建成弱。申请人前期从SR3中鉴定了首个参与蓝光和盐胁迫应答通路的转录抑制因子TaGBF1，其过表达促进蓝光介导的光形态建成，并通过ABA通路关键因子ABI5降低耐盐性，而RNAi相反（与SR3表型一致），但机制还不清楚（Plant J,2015）。进一步鉴定了TaGBF1靶基因TaCKB4，其抑制蓝光介导的光形态建成，也降低耐盐能力；能与蓝光介导的光形态建成通路关键因子HY5互作并影响ABI5表达。本项目拟初步解析TaGBF1-TaCKB4通过HY5调控光形态建成、通过双重调控ABI5降低耐盐性的分子机理，为认识光和盐胁迫信号交互机制提供分子证据，并为小麦（作物）分子育种提供分子元件。

本项目前期从小麦中鉴定了首个参与蓝光和盐胁迫应答通路的转录抑制因子TaGBF1，其过表达促进蓝光介导的光形态建成、降低耐盐能力，但机制还不清楚。本项目在前期基础上，分析了TaGBF1靶基因TaCKB4在蓝光介导的光形态建成及盐胁迫应答中的作用。首先，TaCKB4提高萌发期对盐胁迫和ABA的敏感性，而幼苗期促进了对盐胁迫的抗性，表明该基因在萌发和幼苗阶段的盐胁迫应答中发挥双重作用。TaCKB4能够与TaCKA形成CKII蛋白的四聚体形式，TaCKB4能够结合TaABI4，并介导了TaCKA对TaCKB4和TaABI4的磷酸化，抑制了TaABI4与靶基因启动子的结合能力，降低了TaABI4的转录能力。另一方面，TaCKB4能够与TaSOS2结合，并且改变了离子通道相关基因的表达，表明TaCKB4通过SOS通路调控离子平衡，促进苗期的耐盐能力。此外，TaCKB4与WABI5互作，并且改变蓝光条件下WABI4和HY5的盐胁迫应答水平。本项目初步明确了TaCKB4在蓝光介导的光形态建成和盐胁迫应答中的功能和分子机制，为下一步研究奠定了基础，并且TaCKB4是一个用于分子育种的候选元件。