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内容記述 |
Arabidopsis thaliana has more than 2,000 accessions, showing large variation in salt tolerance. Although several tolerant accessions have been identified, the molecular mechanisms underlying the variation remains largely unknown. To uncover the mechanism, we focused on one of the most salt-tolerant accessions, Lch-0, which exhibits remarkable tolerance to 300 mM NaCl, comparable to the halophyte Eutrema salsugineum. Genetic analysis revealed that an insertion of several hundred base pairs occurred in a gene, designed as SALT located within the causal locus of Lch-0. A Col-0–background salt mutant showed markedly enhanced salt tolerance compared to the wild type, suggesting that Lch-0 enhances the salt tolerance through loss-of-function of the SALT gene. Imaging analysis using radioisotope rebelled 22Na shows the accumulation of 22Na in leaves was lower in salt mutant compared to the WT, demonstrating Na-accumulation confers to salt tolerance among these accessions, and the SALT gene is involved in transportation of Na in above ground tissue. Micro-PIXE analysis indicated that the SALT gene promotes sodium transport from vascular bundles to mesophyll cells. |