Division of Applied Life Science (BK21 program) and Environmental BiotechnologyNational Core Research Center, Graduate School of Gyeongsang NationalUniversity, Jinju 660-701, Korea.
J Exp Bot. 2010 Feb;61(4):1205-13. doi: 10.1093/jxb/erp391. Epub 2010 Jan 6.
A mutation of AtSOS1 (Salt Overly Sensitive 1), a plasma membrane Na(+)/H(+)-antiporter in Arabidopsis thaliana, leads to a salt-sensitive phenotype accompanied by the death of root cells under salt stress. Intracellular events and changes in gene expression were compared during a non-lethal salt stress between the wild type and a representative SOS1 mutant, atsos1-1, by confocal microscopy using ion-specific fluorophores and by quantitative RT-PCR. In addition to the higher accumulation of sodium ions, atsos1-1 showed inhibition of endocytosis, abnormalities in vacuolar shape and function, and changes in intracellular pH compared to the wild type in root tip cells under stress. Quantitative RT-PCR revealed a dramatically faster and higher induction of root-specific Ca(2+) transporters, including several CAXs and CNGCs, and the drastic down-regulation of genes involved in pH-homeostasis and membrane potential maintenance. Differential regulation of genes for functions in intracellular protein trafficking in atsos1-1 was also observed. The results suggested roles of the SOS1 protein, in addition to its function as a Na(+)/H(+) antiporter, whose disruption affected membrane traffic and vacuolar functions possibly by controlling pH homeostasis in root cells.
拟南芥质膜 Na(+)/H(+)反向转运蛋白 AtSOS1（盐过度敏感 1）的突变导致盐敏感表型，并在盐胁迫下导致根细胞死亡。通过使用离子特异性荧光探针和定量 RT-PCR，在非致死性盐胁迫下，通过共聚焦显微镜比较了野生型和代表性 SOS1 突变体 atsos1-1 之间的细胞内事件和基因表达变化。与野生型相比，atsos1-1 在根尖端细胞中除了钠离子积累更高外，还表现出内吞作用抑制、液泡形状和功能异常以及细胞内 pH 变化。定量 RT-PCR 显示，根特异性 Ca(2+)转运蛋白（包括几个 CAXs 和 CNGCs）的诱导更快、更高，参与 pH 稳态和膜电位维持的基因急剧下调。在 atsos1-1 中还观察到细胞内蛋白质运输功能基因的差异调节。结果表明 SOS1 蛋白的作用不仅与其作为 Na(+)/H(+)反向转运蛋白的功能有关，其功能障碍还可能通过控制根细胞的 pH 稳态来影响膜运输和液泡功能。
