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Published online 31 January 2005
Published in Crop Sci 45:437-448 (2005)
© 2005 Crop Science Society of America
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Understanding and Improving Salt Tolerance in Plants

Viswanathan Chinnusamya, André Jagendorfb and Jian-Kang Zhuc,*

a Water Technology Centre, Indian Agricultural Research Institute, New Delhi, India
b Department of Plant Biology, Cornell University, Ithaca, NY14853
c Institute for Integrative Genome Biology and Department of Botany and Plant Sciences, University of California, Riverside, California 92521


Figure 1
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  		Fig. 1. SOS signaling pathway for ion homeostasis under salt stress in Arabidopsis. Salt stress elicited Ca2+ signals are perceived by SOS3, which activates the protein kinase SOS2. Activated SOS2 phosphorylates SOS1, a plasma membrane Na+/H+ antiporter, which then transports Na+ out of the cytosol. The transcript level of SOS1 is regulated by the SOS3-SOS2 kinase complex. SOS2 also activates the tonoplast Na+/H+ antiporter that sequesters Na+ into the vacuole. Na+ entry into the cytosol through the Na+ transporter HKT1 may also be restricted by SOS2. ABI1 regulates the gene expression of NHX1, while ABI2 interacts with SOS2 and negatively regulates ion homeostasis either by inhibiting SOS2 kinase activity or the activities of SOS2 targets. Double arrow indicates SOS3-independent and SOS2-dependent pathway.

 

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  		Fig. 2. LEA-type gene transcription under abiotic stresses in Arabidopsis. ABA-independent DREB2 and ABA-dependent CBF4 transcription factors transactivate DRE/CRT cis-elements in the promoters of LEA type genes. ABA-dependent pathways regulate LEA type genes through MYC/MYB and bZIP type transcription factors. ABA-dependent signaling is mediated through IP3 and Ca2+. FRY1 negatively regulates IP3 levels. ABA induced Ca2+ signaling is negatively regulated by ABI1/2 protein phosphatase 2C. Low temperature stress activates ICE1 a myc-like bHLH transcription factor, which binds to myc type cis-elements of CBF3 promoter and induces CBF3 expression. CBFs bind to the CRT/DRE cis-elements on the promoter of LEA-type genes and induce expression of these genes.

 




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