Horie Tomoaki, Motoda Jo, Kubo Masahiro, Yang Hua, Yoda Kinya, Horie Rie, Chan Wai-Yin, Leung Ho-Yin, Hattori Kazumi, Konomi Mami, Osumi Masako, Yamagami Mutsumi, Schroeder Julian I, Uozumi Nobuyuki
Bioscience and Biotechnology Center, Nagoya University, Nagoya 464-8601, Japan.
Plant J. 2005 Dec;44(6):928-38. doi: 10.1111/j.1365-313X.2005.02595.x.
AtHKT1 is a sodium (Na+) transporter that functions in mediating tolerance to salt stress. To investigate the membrane targeting of AtHKT1 and its expression at the translational level, antibodies were generated against peptides corresponding to the first pore of AtHKT1. Immunoelectron microscopy studies using anti-AtHKT1 antibodies demonstrate that AtHKT1 is targeted to the plasma membrane in xylem parenchyma cells in leaves. AtHKT1 expression in xylem parenchyma cells was also confirmed by AtHKT1 promoter-GUS reporter gene analyses. Interestingly, AtHKT1 disruption alleles caused large increases in the Na+ content of the xylem sap and conversely reduced the Na+ content of the phloem sap. The athkt1 mutant alleles had a smaller and inverse influence on the potassium (K+) content compared with the Na+ content of the xylem, suggesting that K+ transport may be indirectly affected. The expression of AtHKT1 was modulated not only by the concentrations of Na+ and K+ but also by the osmolality of non-ionic compounds. These findings show that AtHKT1 selectively unloads sodium directly from xylem vessels to xylem parenchyma cells. AtHKT1 mediates osmolality balance between xylem vessels and xylem parenchyma cells under saline conditions. Thus AtHKT1 reduces the sodium content in xylem vessels and leaves, thereby playing a central role in protecting plant leaves from salinity stress.
AtHKT1是一种钠（Na+）转运蛋白，在介导对盐胁迫的耐受性中发挥作用。为了研究AtHKT1的膜靶向作用及其在翻译水平上的表达，制备了针对与AtHKT1第一个孔相对应的肽段的抗体。使用抗AtHKT1抗体的免疫电子显微镜研究表明，AtHKT1定位于叶片木质部薄壁细胞的质膜上。AtHKT1启动子-GUS报告基因分析也证实了AtHKT1在木质部薄壁细胞中的表达。有趣的是，AtHKT1缺失等位基因导致木质部汁液中Na+含量大幅增加，反之则降低了韧皮部汁液中Na+的含量。与木质部的Na+含量相比，athkt1突变等位基因对钾（K+）含量的影响较小且相反，这表明K+运输可能受到间接影响。AtHKT1的表达不仅受到Na+和K+浓度的调节，还受到非离子化合物渗透压的调节。这些发现表明，AtHKT1直接将钠从木质部导管选择性卸载到木质部薄壁细胞中。在盐胁迫条件下，AtHKT1介导木质部导管和木质部薄壁细胞之间的渗透压平衡。因此，AtHKT1降低了木质部导管和叶片中的钠含量，从而在保护植物叶片免受盐胁迫方面发挥核心作用。
