4.7 Article

Intracellular consequences of SOS1 deficiency during salt stress

期刊

JOURNAL OF EXPERIMENTAL BOTANY
卷 61, 期 4, 页码 1205-1213

出版社

OXFORD UNIV PRESS
DOI: 10.1093/jxb/erp391

关键词

Arabidopsis thaliana; endocytosis; salinity tolerance; SOS1

资金

  1. World Class University [R32-10148]
  2. Environmental Biotechnology National Core Research Center Project [R15-2003-012-01002-00]
  3. Rural Development Administration, Korea [20070301034030]
  4. UIUC
  5. Purdue University
  6. Rural Development Administration (RDA), Republic of Korea [20070301034030] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

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 Ca2+ 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.

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