Sci. STKE, 3 October 2000
Plant Biology Salt Tolerance Requires Myristoylation
Mutations in the SOS3 gene, which is predicted to encode a calcium-binding protein, result in Arabidopsis that cannot tolerate salt stress. SOS3 was myristoylated in vitro. Mutation of the consensus glycine abolished the in vitro myristoylation and abolished the ability of SOS3 to restore salt tolerance to sos3 mutants. Although myristoylation appears essential for SOS3 function, changes in the subcellular distribution or membrane association were not detected between the myristoylation-competent wild type and the glycine to alanine mutant. The sequence of SOS3 predicts an EF-hand calcium-binding domain. Bacterially expressed SOS3 binds calcium with low affinity, and this binding activity is lost in SOS with mutations in the EF-hand domain. The EF-hand mutant SOS does not bind to the downstream kinase SOS2 in yeast two-hybrid assays and does not stimulate SOS2 kinase activity. Thus, SOS3 requires myristoylation and integrity of the EF-hand domain for activity. SOS3 may be regulated by a calcium-myristoyl switch mechanism similar to that described for members of the animal neuronal calcium sensor family of proteins.
Ishitani, M., Liu, J., Halfter, U., Kim, C.-S., Shi, W., and Zhu, J.-K. (2000) SOS2 function in plant salt tolerance requires N-myristoylation and calcium binding. Plant Cell 12: 1667-1677. [Abstract] [Full Text]
Citation: Salt Tolerance Requires Myristoylation. Sci. STKE 2000, tw6 (2000).
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