A retrotransposon in an HKT1 family sodium transporter causes variation of leaf Na + exclusion and salt tolerance in maize.

Soil salinity is one of several major abiotic stresses that constrain maize productivity worldwide. An improved understanding of salt-tolerance mechanisms will thus enhance the breeding of salt-tolerant maize and boost productivity. Previous studies have indicated that the maintenance of leaf Na ⁺ concentration is essential for maize salt tolerance, and the difference in leaf Na ⁺ exclusion has previously been associated with variation in salt tolerance between maize varieties. Here, we report the identification and functional characterization of a maize salt-tolerance quantitative trait locus (QTL), Zea mays Na ⁺ Content1 (ZmNC1), which encodes an HKT-type transporter (designated as ZmHKT1). We show that a natural ZmHKT1 loss-of-function allele containing a retrotransposon insertion confers increased accumulation of Na ⁺ in leaves, and salt hypersensitivity. We next show that ZmHKT1 encodes a plasma membrane-localized Na ⁺ -selective transporter, and is preferentially expressed in root stele (including the parenchyma cells surrounding the xylem vessels). We also show that loss of ZmHKT1 function increases xylem sap Na ⁺ concentration and causes increased root-to-shoot Na ⁺ delivery, indicating that ZmHKT1 promotes leaf Na ⁺ exclusion and salt tolerance by withdrawing Na ⁺ from the xylem sap. We conclude that ZmHKT1 is a major salt-tolerance QTL and identifies an important new gene target in breeding for improved maize salt tolerance.
(© 2017 The Authors. New Phytologist © 2017 New Phytologist Trust.)