Patellin1 Negatively Modulates Salt Tolerance by Regulating PM Na+/H+ Antiport Activity and Cellular Redox Homeostasis in Arabidopsis
Patellin1 Negatively Modulates Salt Tolerance by Regulating PM Na+/H+ Antiport Activity and Cellular Redox Homeostasis in Arabidopsis
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DOI：
10.1093/pcp/pcy081
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发表时间：
2018-08
影响因子：
4.9
通讯作者：
Huapeng Zhou;Chongwu Wang;Tinghong Tan;Jingqing Cai;Jiaxian He;Honghui Lin
中科院分区：
文献类型：
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作者：
Huapeng Zhou;Chongwu Wang;Tinghong Tan;Jingqing Cai;Jiaxian He;Honghui Lin
土壤盐分对植物的发育和生长有显著的抑制作用。钠离子（Na+）的挤压和区隔、细胞膜内运输以及氧化还原稳态调节等机制在植物耐盐性中起着重要作用。在这项研究中，我们报道了Patellin1 (PATL1)，一种膜运输相关蛋白，调节拟南芥的耐盐性。PATL1的T-DNA插入突变体（PATL1）具有较高的PATL1转录水平，显示出盐敏感表型。PATL1部分与质膜（PM）和内体系统相关，并可能参与调节膜运输。有趣的是，PATL1与盐过度敏感（SOS）途径中的PM Na+/H+反转运蛋白SOS1相互作用，并且PATL1中的PM Na+/H+反转运活性低于Col-0。此外，在盐胁迫条件下，patl1中活性氧（ROS）含量较高，抗氧化剂的氧化还原信号被部分破坏。人工消除ROS可以部分恢复patl1的盐敏感表型。综上所述，我们的研究结果表明，PATL1至少部分通过SOS1调节Na+运输，并在盐胁迫下调节细胞氧化还原稳态，从而参与植物耐盐性。
Soil salinity significantly represses plant development and growth. Mechanisms involved sodium (Na+) extrusion and compartmentation, intracellular membrane trafficking as well as redox homeostasis regulation play important roles in plant salt tolerance. In this study, we report that Patellin1 (PATL1), a membrane trafficking-related protein, modulates salt tolerance in Arabidopsis. The T-DNA insertion mutant of PATL1 (patl1) with an elevated PATL1 transcription level displays a salt-sensitive phenotype. PATL1 partially associates with the plasma membrane (PM) and endosomal system, and might participate in regulating membrane trafficking. Interestingly, PATL1 interacts with SOS1, a PM Na+/H+ antiporter in the Salt-Overly-Sensitive (SOS) pathway, and the PM Na+/H+ antiport activity is lower in patl1 than in Col-0. Furthermore, the reactive oxygen species (ROS) content is higher in patl1 and the redox signaling of antioxidants is partially disrupted in patl1 under salt stress conditions. Artificial elimination of ROS could partially rescue the salt-sensitive phenotype of patl1. Taken together, our results indicate that PATL1 participates in plant salt tolerance by regulating Na+ transport at least in part via SOS1, and by modulating cellular redox homeostasis during salt stress.