title: AtHKT1 facilitates Na+ homeostasis and K+ nutrition in planta.
abstract: Genetic and physiological data establish that Arabidopsis AtHKT1 facilitates Na(+) homeostasis in planta and by this function modulates K(+) nutrient status. Mutations that disrupt AtHKT1 function suppress NaCl sensitivity of sos1-1 and sos2-2, as well as of sos3-1 seedlings grown in vitro and plants grown in controlled environmental conditions. hkt1 suppression of sos3-1 NaCl sensitivity is linked to higher Na(+) content in the shoot and lower content of the ion in the root, reducing the Na(+) imbalance between these organs that is caused by sos3-1. AtHKT1 transgene expression, driven by its innate promoter, increases NaCl but not LiCl or KCl sensitivity of wild-type (Col-0 gl1) or of sos3-1 seedlings. NaCl sensitivity induced by AtHKT1 transgene expression is linked to a lower K(+) to Na(+) ratio in the root. However, hkt1 mutations increase NaCl sensitivity of both seedlings in vitro and plants grown in controlled environmental conditions, which is correlated with a lower K(+) to Na(+) ratio in the shoot. These results establish that AtHKT1 is a focal determinant of Na(+) homeostasis in planta, as either positive or negative modulation of its function disturbs ion status that is manifested as salt sensitivity. K(+)-deficient growth of sos1-1, sos2-2, and sos3-1 seedlings is suppressed completely by hkt1-1. AtHKT1 transgene expression exacerbates K(+) deficiency of sos3-1 or wild-type seedlings. Together, these results indicate that AtHKT1 controls Na(+) homeostasis in planta and through this function regulates K(+) nutrient status.
authors.affiliation: Center for Plant Environmental Stress Physiology, Purdue University, West Lafayette, IN 47907-2010, USA.
authors.forename: Ana
authors.initials: A
authors.lastname: Rus
authors.forename: Byeong-ha
authors.initials: BH
authors.lastname: Lee
authors.forename: Alicia
authors.initials: A
authors.lastname: Muñoz-Mayor
authors.forename: Altanbadralt
authors.initials: A
authors.lastname: Sharkhuu
authors.forename: Kenji
authors.initials: K
authors.lastname: Miura
authors.forename: Jian-Kang
authors.initials: JK
authors.lastname: Zhu
authors.forename: Ray A
authors.initials: RA
authors.lastname: Bressan
authors.forename: Paul M
authors.initials: PM
authors.lastname: Hasegawa
mesh_terms: D017360:Arabidopsis / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism*; D001483:Base Sequence; D027682:Cation Transport Proteins / Q000235:genetics / Q000378:metabolism*; D018744:DNA, Plant / Q000235:genetics; D017343:Genes, Plant; D006706:Homeostasis; D008969:Molecular Sequence Data; D009154:Mutation; D009747:Nutritional Physiological Phenomena; D011188:Potassium / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000235:genetics; D013014:SOS Response, Genetics; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride / Q000494:pharmacology; D017923:Sodium-Hydrogen Exchangers / Q000235:genetics; D013489:Suppression, Genetic; D027981:Symporters / Q000235:genetics / Q000378:metabolism*
chemical_list: D029681:Arabidopsis Proteins; D027682:Cation Transport Proteins; D018744:DNA, Plant; C490286:HKT1 protein, Arabidopsis; C477653:SOS1 protein, Arabidopsis; C112941:SOS3 protein, Arabidopsis; D017923:Sodium-Hydrogen Exchangers; D027981:Symporters; D012965:Sodium Chloride; D012964:Sodium; C406738:SOS2 protein, Arabidopsis; D017346:Protein Serine-Threonine Kinases; D011188:Potassium