title: Enhanced salt tolerance mediated by AtHKT1 transporter-induced Na unloading from xylem vessels to xylem parenchyma cells.
abstract: 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.
authors.affiliation: Bioscience and Biotechnology Center, Nagoya University, Nagoya 464-8601, Japan.
authors.lastname: Sunarpi
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Horie
authors.forename: Jo
authors.initials: J
authors.lastname: Motoda
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kubo
authors.forename: Hua
authors.initials: H
authors.lastname: Yang
authors.forename: Kinya
authors.initials: K
authors.lastname: Yoda
authors.forename: Rie
authors.initials: R
authors.lastname: Horie
authors.forename: Wai-Yin
authors.initials: WY
authors.lastname: Chan
authors.forename: Ho-Yin
authors.initials: HY
authors.lastname: Leung
authors.forename: Kazumi
authors.initials: K
authors.lastname: Hattori
authors.forename: Mami
authors.initials: M
authors.lastname: Konomi
authors.forename: Masako
authors.initials: M
authors.lastname: Osumi
authors.forename: Mutsumi
authors.initials: M
authors.lastname: Yamagami
authors.forename: Julian I
authors.initials: JI
authors.lastname: Schroeder
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Uozumi
mesh_terms: D017360:Arabidopsis / Q000166:cytology / Q000235:genetics / Q000378:metabolism*; D029681:Arabidopsis Proteins / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D001692:Biological Transport; D027682:Cation Transport Proteins / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D002462:Cell Membrane / Q000737:chemistry / Q000378:metabolism; D018506:Gene Expression Regulation, Plant; D017930:Genes, Reporter; D005816:Genetic Complementation Test; D008954:Models, Biological; D009994:Osmolar Concentration; D018515:Plant Leaves / Q000033:anatomy & histology / Q000378:metabolism; D030821:Plants, Genetically Modified / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*; D027981:Symporters / Q000032:analysis / Q000235:genetics / Q000502:physiology*
chemical_list: D029681:Arabidopsis Proteins; D027682:Cation Transport Proteins; C490286:HKT1 protein, Arabidopsis; D027981:Symporters; D012964:Sodium; D011188:Potassium