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J Exp Bot. 2010 Feb;61(4):1205-13. doi: 10.1093/jxb/erp391. Epub 2010 Jan 6.

Intracellular consequences of SOS1 deficiency during salt stress.

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1
Division of Applied Life Science (BK21 program) and Environmental BiotechnologyNational Core Research Center, Graduate School of Gyeongsang NationalUniversity, Jinju 660-701, Korea.

Abstract

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.

PMID:
20054031
PMCID:
PMC2826659
DOI:
10.1093/jxb/erp391
[Indexed for MEDLINE]
Free PMC Article
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