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 μM 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 .