Guangdong Provincial Key Laboratory for Plant Epigenetics, Longhua Bioindustry and Innovation Research Institute, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518060, China.
Key Laboratory of Optoelectronic Devices and Systems of Ministry of Education and Guangdong Province, College of Optoelectronic Engineering, Shenzhen University, Shenzhen 518060, China.
Int J Mol Sci. 2023 Jun 6;24(12):9793. doi: 10.3390/ijms24129793.
Plants have evolved diverse strategies to accommodate saline environments. More insights into the knowledge of salt stress regulatory pathways will benefit crop breeding. RADICAL-INDUCED CELL DEATH 1 (RCD1) was previously identified as an essential player in salt stress response. However, the underlying mechanism remains elusive. Here, we unraveled that NAC domain-containing protein 17 (ANAC017) acts downstream of RCD1 in salt stress response, and its ER-to-nucleus transport is triggered by high salinity. Genetic and biochemical evidence showed that RCD1 interacts with transmembrane motif-truncated ANAC017 in the nucleus and represses its transcriptional activity. Transcriptome analysis revealed that genes associated with oxidation reduction process and response to salt stress are similarly dysregulated in loss-of-function and gain-of-function mutants. In addition, we found that ANAC017 plays a negative role in salt stress response by impairing the superoxide dismutase (SOD) enzyme activity. Taken together, our study uncovered that RCD1 promotes salt stress response and maintains ROS homeostasis by inhibiting ANAC017 activity.
植物已经进化出多种策略来适应盐环境。更多地了解盐胁迫调控途径的知识将有助于作物的培育。RADICAL-INDUCED CELL DEATH 1(RCD1)先前被鉴定为盐胁迫反应中的一个重要参与者。然而,其潜在的机制仍不清楚。在这里,我们揭示了含有 NAC 结构域的蛋白 17(ANAC017)在盐胁迫反应中作为 RCD1 的下游分子,其内质网到细胞核的运输是由高盐度触发的。遗传和生化证据表明,RCD1 在核内与跨膜结构域缺失的 ANAC017 相互作用,并抑制其转录活性。转录组分析表明,与氧化还原过程和盐胁迫反应相关的基因在功能缺失和功能获得突变体中同样失调。此外,我们发现 ANAC017 通过损害超氧化物歧化酶(SOD)酶活性,在盐胁迫反应中起负作用。总之,我们的研究揭示了 RCD1 通过抑制 ANAC017 的活性来促进盐胁迫反应和维持 ROS 平衡。