非生物胁迫会严重影响植物生长，造成作物减产。多种非生物胁迫都会引起活性氧的积累，而活性氧会激活MAPK信号级联途径，使植物快速响应非生物胁迫。活性氧引发的MAPK信号通路的激活对于植物响应多种胁迫起到重要作用，但活性氧激活MAPK通路的过程中是否存在其他因子的精细调控，这一问题还有待深入研究。本项目的前期工作发现一个拟南芥RING型锌指蛋白突变体nca1-3对盐碱胁迫、氧化胁迫、低温胁迫多种非生物胁迫具有敏感表型，并且突变体中过氧化氢含量高于野生型；质谱检测发现NCA1与MPK3、MPK6相互作用；NCA1的缺失使活性氧引起的MPK3、MPK6激活发生延迟。本项目拟深入研究NCA1调控活性氧激活MPK3、MPK6的分子机制，进一步阐明活性氧激活的MAPK信号通路的调节方式，完善植物通过MAPK通路调控多种逆境响应的机制，为耐逆境农作物新品种培育提供理论基础。

Abiotic stresses impact plant growth severely and lead to a reduction in grain yield. Multiple abiotic stresses lead to accumulation of Reactive Oxygen Species, which activates MAPK signaling pathway and finally responds to multiple stresses. ROS-induced activation of MAPK cascades plays an important role in response to multiple abiotic stresses. However, it is not clear whether other regulators work in ROS-induced MAPK activation. Our previous work found an Arabidopsis mutant nca1-3, in which the gene encodes a RING finger protein NCA1 is mutated, shows sensitive phenotype to saline stress, alkaline stress, oxidative stress and cold stress. Besides, the hydrogen peroxide content in nca1-3 mutant is higher than that in wildtype. NCA1 interacting protein MPK3 and MPK6 were identified by Mass spectrum. Loss function of NCA1 leads to a delay of MPK3/MPK6 kinase activation under ROS treatment. We will further study on the mechanism of NCA1 regulation on ROS-activated MPK3/MPK6 activity. Our study will further illuminate the regulation of ROS-activated MAPK signaling pathway and consummate the mechanism of MAPK-involved response to multiple abiotic stresses in plant. Therefore, this work will provide theoretical basis for breeding development of stress-resistant crops.