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

Summary 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 ( Zm NC 1 ), which encodes an HKT ‐type transporter (designated as Zm HKT 1 ). We show that a natural Zm HKT 1 loss‐of‐function allele containing a retrotransposon insertion confers increased accumulation of Na + in leaves, and salt hypersensitivity. We next show that Zm HKT 1 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 Zm HKT 1 function increases xylem sap Na + concentration and causes increased root‐to‐shoot Na + delivery, indicating that Zm HKT 1 promotes leaf Na + exclusion and salt tolerance by withdrawing Na + from the xylem sap. We conclude that Zm HKT 1 is a major salt‐tolerance QTL and identifies an important new gene target in breeding for improved maize salt tolerance.