AtHKT1 is a salt tolerance determinant that controls Na+ entry into plant roots

Two Arabidopsis thaliana extragenic mutations that suppress NaCl hypersensi tivity of the sos3-1 mutant were identified in a screen of a T-DNA insertio n 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 tha t 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 i s not detected in plants of either mutant, indicating that this gene is ina ctivated by the mutations. hkt1-1 and hkt1-2 mutations can suppress to an e quivalent extent the Na+ sensitivity of sos3-1 seedlings and reduce the int racellular accumulation of this cytotoxic ion. Moreover, sos3-1 hkt1-1 and sos3-1 hkt1-2 seedlings are able to maintain [K+](int) in medium supplement ed with NaCl and exhibit a substantially higher intracellular ratio of K+/N a+ than the sos3-1 mutant. Furthermore, the hkt1 mutations abrogate the gro wth inhibition of the sos3-1 mutant that is caused by K+ deficiency on cult ure medium with low Ca2+ (0.15 mM) and < 200 muM K+. Interestingly, the cap acity of hkt1 mutations to suppress the Na+ hypersensitivity of the sos3-1 mutant is reduced substantially when seedlings are grown in medium with low Ca2+ (0.15 mM). These results indicate that AtHKT1 is a salt tolerance det erminant that controls Na+ entry and high affinity K+ uptake. The hkt1 muta tions have revealed the existence of another Na+ influx system(s) whose act ivity is reduced by high [Ca2+](ext).