CO转录因子调控拟南芥茉莉酸激素信号转导的分子机理

CO转录因子是光周期途径调控拟南芥开花过程的关键决定因子。CO除了在幼叶微管组织表达促进开花，还在幼叶叶肉细胞及根部强表达，但功能未知。我们近期发现CO的转录受茉莉酸（JA）抑制，并且CO能负调控JA反应。CO特异与JA途径重要转录因子bHLH3和bHLH17互作，且它们具有类似生物学功能。上述结果暗示CO可能通过与bHLH3和bHLH17互作协同抑制JA反应。为了深入研究CO-bHLH复合物调控JA反应的分子机理，本项目将采用分子生物学、遗传学及生物化学的方法手段，证实CO和bHLH3/bHLH17之间的遗传关系，详细分析它们是否影响对方的DNA结合能力、转录调控功能或蛋白稳定性等，明确光周期信号是否调控JA反应。本项目的研究结果不仅有望发现CO新的生物学功能，还有可能在分子水平阐明CO作为关键节点整合光周期与JA信号，这对于深入理解外源环境信号与JA信号交互的分子机理具有重要科学意义。

CONSTANS (CO) transcription factor is a critical regulator of photoperiodic flowering in Arabidopsis. CO is widely expressed in multiple tissues, such as in young leaves and roots of seedlings, but little is known about the regulatory functions and underlying molecular mechanisms of CO in modulating other physiological processes in addition to flowering. Recently, we found that the transcription of CO is repressed by the phytohormone jasmonate (JA). CO negatively modulates JA-signaled root growth inhibition and anthocyanin accumulation. Disrupting CO rendered seedlings more sensitive to JA, whereas overexpression of CO resulted in plants with reduced JA sensitivity. CO physically associates with basic helix-loop-helix (bHLH) subgroup IIId factors bHLH3 and bHLH17. Moreover, CO may synergize with bHLH3/bHLH17 in JA signaling. These results suggest that CO may interact with bHLH3/bHLH17 to negatively regulate JA signaling. To test this possibility, we will undertake molecular and genetic approaches in this project to further clarify the genetic interactions between CO and bHLH3/bHLH17 in JA signaling. Furthermore, we will analyze whether CO and bHLH3/bHLH17 reciprocally affect each other’s DNA-binding activity, transcriptional function, and/or degradation. In addition, we will investigate the potential roles of photoperiodic signal in mediating JA responses. Collectively, our study may not only contribute to reveal key functions of CO and photoperiodic signal in regulating JA responses, but also provides a mechanistic explanation of how CO acts together with bHLH3/bHLH17 factors to integrate photoperiod pathway and JA signaling.