Song Ru-Feng, Liao Cai-Yi, Wang Lin-Feng, Lu Kai-Kai, Zhang Chi, Wu Run-Xin, Wu Ji-Xiao, Ma Yu-Qing, Kuang Lei, Guo Ning, Yuan Hong-Mei, Liu Wen-Cheng
State Key Laboratory of Crop Stress Adaptation and Improvement, Collaborative Innovation Center of Crop Stress Biology, College of Life Sciences, Henan University, Kaifeng 475004, China.
Sanya Institute of Henan University, Sanya 572025, China.
Plant Physiol. 2024 Dec 23;197(1). doi: 10.1093/plphys/kiae633.
The plasma membrane (PM)-localized Na+/H+ antiporter Salt Overly Sensitive1 (SOS1) is essential for plant salt tolerance through facilitating Na+ efflux; however, how SOS1 localization and protein accumulation is regulated in plants remains elusive. Here, we report that Sorting Nexin 1 (SNX1) is required for plant salt-stress tolerance through affecting endosomal trafficking of SOS1 in Arabidopsis (Arabidopsis thaliana). Disruption of SNX1 caused salt hypersensitivity with increased Na+ accumulation and decreased Na+ efflux in Arabidopsis when challenged with high salinity stress. SNX1 co-localized and interacted with SOS1 in endosomes, promoting its PM localization and protein stability in plants under saline conditions. SOS1 overexpression promoted salt tolerance in the wild-type, whereas such effect was greatly compromised in the snx1-2 mutant. Pharmaceutical results showed that SOS1 recycling from the cytosol to the PM was largely blocked while its vacuolar degradation was accelerated in the snx1-2 mutant. Furthermore, salt-induced SOS1 phosphorylation enhanced its interaction and co-localization with SNX1, which is required for SOS1 PM localization in plants. Our study elucidates that SNX1 facilitates SOS1 PM localization and protein accumulation through endosomal trafficking, thereby enhancing salt tolerance in plants.
质膜(PM)定位的Na⁺/H⁺逆向转运蛋白盐过度敏感1(SOS1)通过促进Na⁺外流对植物耐盐性至关重要;然而,SOS1在植物中的定位和蛋白质积累是如何调控的仍不清楚。在这里,我们报道分拣连接蛋白1(SNX1)通过影响拟南芥中SOS1的内体运输对植物耐盐胁迫是必需的。在高盐胁迫下,SNX1的破坏导致拟南芥盐超敏,Na⁺积累增加,Na⁺外流减少。SNX1在内体中与SOS1共定位并相互作用,在盐胁迫条件下促进其在植物中的质膜定位和蛋白质稳定性。SOS1过表达促进野生型的耐盐性,而在snx1-2突变体中这种效应大大受损。药理学结果表明,在snx1-2突变体中,SOS1从细胞质到质膜的循环在很大程度上被阻断,而其液泡降解加速。此外,盐诱导的SOS1磷酸化增强了其与SNX1的相互作用和共定位,这是植物中SOS1质膜定位所必需的。我们的研究阐明,SNX1通过内体运输促进SOS1的质膜定位和蛋白质积累,从而增强植物的耐盐性。