Received April 17, 2007
Accepted June 18, 2007
Rice Shaker Potassium Channel OsKAT1 Confers Tolerance to Salinity Stress on Yeast and Rice Cells
Toshihiro Obata , Hiroko K. Kitamoto , Atsuko Nakamura , Atsunori Fukuda , and Yoshiyuki Tanaka *
Division of Plant Sciences, National Institute of Agrobiological Sciences, Tsukuba 305-8602, Japan; Environmental Biofunction Division, National Institute for Agro-Environmental Sciences, Tsukuba 305-8604, Japan
* Corresponding author; email: tanakayo{at}affrc.go.jp.
We screened a rice (Oryza sativa L. cv. Nipponbare) full-length cDNA expression library through functional complementation in yeast (Saccharomyces cerevisiae) to find novel cation transporters involved in salt tolerance. We found that expression of a cDNA clone, encoding the rice homologue of Shaker family K+ channel KAT1 (OsKAT1), suppressed the salt-sensitive phenotype of yeast strain G19 (
ena1-4), which lacks a major component of Na+ efflux. It also suppressed a K+-transport-defective phenotype of yeast strain CY162 (
trk1
trk2), suggesting the enhancement of K+ uptake by OsKAT1. By the expression of OsKAT1, the K+ contents of salt-stressed G19 cells increased during the exponential growth phase. At the linear phase, however, OsKAT1-expressing G19 cells accumulated less Na+ than non-expressing cells, but almost the same K+. The cellular Na+:K+ ratio of OsKAT1-expressing G19 cells remained lower than non-expressing cells under saline conditions. Rice cells overexpressing OsKAT1 also showed enhanced salt tolerance and increased cellular K+ content. These functions of OsKAT1 are likely to be common among Shaker K+ channels because OsAKT1 and Arabidopsis KAT1 were able to complement the salt-sensitive phenotype of G19 as well as OsKAT1. The expression of OsKAT1 was restricted to internodes and rachides of wild-type rice, whereas other Shaker family genes were expressed in various organs. These results suggest that OsKAT1 is involved in salt tolerance of rice in cooperation with other K+ channels by participating in maintenance of cytosolic cation homeostasis during salt stress, and thus protects cells from Na+.