Liu Guoyong, Zeng Yonglun, Li Baiying, Wang Xiangfeng, Jiang Liwen, Guo Yan
State Key Laboratory of Plant Environmental Resilience, China Agricultural University, Beijing 100193, China.
State Key Laboratory of Plant Diversity and Specialty Crops and Guangdong Provincial Key Laboratory of Applied Botany, South China Botanical Garden, Chinese Academy of Sciences, Guangzhou 510650, China.
Plant Cell. 2025 Mar 5;37(3). doi: 10.1093/plcell/koaf012.
Salt stress causes ion toxicity in plant cells and limits plant growth and crop productivity. Sodium ions (Na+) are transported out of the cell and sequestered in the vacuole for detoxification under salt stress. The salt excretion system is controlled by the SALT OVERLY SENSITIVE (SOS) pathway, which consists of the calcium sensors SOS3 and SOS3-LIKE CALCIUM-BINDING PROTEIN 8, the protein kinase SOS2, and the plasma membrane Na+/H+ antiporter SOS1. Although much is known about salt responses in plants at the molecular level, it remains unclear if and how plants respond to salt stress through endomembrane remodelling. In this study, we describe a mechanism of salt tolerance in Arabidopsis (Arabidopsis thaliana) involving the modulation of FREE1 levels, which impacts multivesicular body (MVB) trafficking. Specifically, the ESCRT-I (endosomal sorting complex required for transport-I) component FREE1 (FYVE DOMAIN PROTEIN REQUIRED FOR ENDOSOMAL SORTING 1) regulates vacuole fragmentation to enhance salt tolerance. SOS2 phosphorylates FREE1, leading to its degradation and affecting MVB maturation, thereby reducing MVB-vacuole fusion and regulating endomembrane dynamics in response to salt stress. These findings highlight the adaptive role of the plant endomembrane system in coping with salt stress.
盐胁迫会导致植物细胞中的离子毒性,并限制植物生长和作物产量。在盐胁迫下,钠离子(Na+)会被转运出细胞并隔离在液泡中进行解毒。盐排泄系统受盐过度敏感(SOS)途径控制,该途径由钙传感器SOS3和类SOS3钙结合蛋白8、蛋白激酶SOS2以及质膜Na+/H+逆向转运蛋白SOS1组成。尽管在分子水平上对植物的盐反应已有很多了解,但尚不清楚植物是否以及如何通过内膜重塑来应对盐胁迫。在本研究中,我们描述了拟南芥中一种耐盐机制,该机制涉及FREE1水平的调节,这会影响多泡体(MVB)运输。具体而言,ESCRT-I(运输所需的内体分选复合体-I)组分FREE1(内体分选所需的FYVE结构域蛋白1)调节液泡碎片化以增强耐盐性。SOS2使FREE1磷酸化,导致其降解并影响MVB成熟,从而减少MVB与液泡的融合并调节内膜动态以应对盐胁迫。这些发现突出了植物内膜系统在应对盐胁迫中的适应性作用。