title: AtHKT1 is a salt tolerance determinant that controls Na(+) entry into plant roots.
abstract: Two Arabidopsis thaliana extragenic mutations that suppress NaCl hypersensitivity of the sos3-1 mutant were identified in a screen of a T-DNA insertion population in the genetic background of Col-0 gl1 sos3-1. Analysis of the genome sequence in the region flanking the T-DNA left border indicated that sos3-1 hkt1-1 and sos3-1 hkt1-2 plants have allelic mutations in AtHKT1. AtHKT1 mRNA is more abundant in roots than shoots of wild-type plants but is not detected in plants of either mutant, indicating that this gene is inactivated by the mutations. hkt1-1 and hkt1-2 mutations can suppress to an equivalent extent the Na(+) sensitivity of sos3-1 seedlings and reduce the intracellular accumulation of this cytotoxic ion. Moreover, sos3-1 hkt1-1 and sos3-1 hkt1-2 seedlings are able to maintain [K(+)](int) in medium supplemented with NaCl and exhibit a substantially higher intracellular ratio of K(+)/Na(+) than the sos3-1 mutant. Furthermore, the hkt1 mutations abrogate the growth inhibition of the sos3-1 mutant that is caused by K(+) deficiency on culture medium with low Ca(2+) (0.15 mM) and <200 microM K(+). Interestingly, the capacity of hkt1 mutations to suppress the Na(+) hypersensitivity of the sos3-1 mutant is reduced substantially when seedlings are grown in medium with low Ca(2+) (0.15 mM). These results indicate that AtHKT1 is a salt tolerance determinant that controls Na(+) entry and high affinity K(+) uptake. The hkt1 mutations have revealed the existence of another Na(+) influx system(s) whose activity is reduced by high [Ca(2+)](ext).
authors.affiliation: Center for Plant Environmental Stress Physiology, Purdue University, West Lafayette, IN 47907-1165, USA.
authors.forename: A
authors.initials: A
authors.lastname: Rus
authors.forename: S
authors.initials: S
authors.lastname: Yokoi
authors.forename: A
authors.initials: A
authors.lastname: Sharkhuu
authors.forename: M
authors.initials: M
authors.lastname: Reddy
authors.forename: B H
authors.initials: BH
authors.lastname: Lee
authors.forename: T K
authors.initials: TK
authors.lastname: Matsumoto
authors.forename: H
authors.initials: H
authors.lastname: Koiwa
authors.forename: J K
authors.initials: JK
authors.lastname: Zhu
authors.forename: R A
authors.initials: RA
authors.lastname: Bressan
authors.forename: P M
authors.initials: PM
authors.lastname: Hasegawa
mesh_terms: D000483:Alleles; D017360:Arabidopsis / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D029681:Arabidopsis Proteins; D002118:Calcium / Q000378:metabolism; D027682:Cation Transport Proteins / Q000235:genetics / Q000378:metabolism*; D002414:Cations, Monovalent; D017343:Genes, Plant; D008094:Lithium; D016296:Mutagenesis; D010641:Phenotype; D010940:Plant Proteins / Q000235:genetics / Q000378:metabolism*; D018517:Plant Roots / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride / Q000494:pharmacology; D027981:Symporters / Q000235:genetics / Q000378:metabolism*
chemical_list: D029681:Arabidopsis Proteins; D027682:Cation Transport Proteins; D002414:Cations, Monovalent; C490286:HKT1 protein, Arabidopsis; C088864:HKT1 protein, plant; D010940:Plant Proteins; C112941:SOS3 protein, Arabidopsis; D027981:Symporters; D012965:Sodium Chloride; D008094:Lithium; D012964:Sodium; D011188:Potassium; D002118:Calcium