Yibo Cao

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.

Abstract Sodium (Na + ) toxicity is one of the major damages imposed on crops by saline-alkaline stress. Here we show that natural maize inbred lines display substantial variations in shoot Na + contents and saline-alkaline (NaHCO 3 ) tolerance, and reveal that ZmNSA1 ( Na + Content under Saline-Alkaline Condition ) confers shoot Na + variations under NaHCO 3 condition by a genome-wide association study. Lacking of ZmNSA1 promotes shoot Na + homeostasis by increasing root Na + efflux. A naturally occurred 4-bp deletion decreases the translation efficiency of ZmNSA1 mRNA, thus promotes Na + homeostasis. We further show that, under saline-alkaline condition, Ca 2+ binds to the EF-hand domain of ZmNSA1 then triggers its degradation via 26S proteasome, which in turn increases the transcripts levels of PM-H + -ATPases ( MHA2 and MHA4 ), and consequently enhances SOS1 Na + /H + antiporter-mediated root Na + efflux. Our studies reveal the mechanism of Ca 2+ -triggered saline-alkaline tolerance and provide an important gene target for breeding saline-alkaline tolerant maize varieties.

Abstract Plant salt-stress response involves complex physiological processes. Previous studies have shown that some factors promote salt tolerance only under high transpiring condition, thus mediating transpiration-dependent salt tolerance (TDST). However, the mechanism underlying crop TDST remains largely unknown. Here, we report that ZmSTL1 ( Salt-Tolerant Locus 1 ) confers natural variation of TDST in maize. ZmSTL1 encodes a dirigent protein (termed ZmESBL) localized to the Casparian strip (CS) domain. Mutants lacking ZmESBL display impaired lignin deposition at endodermal CS domain which leads to a defective CS barrier. Under salt condition, mutation of ZmESBL increases the apoplastic transport of Na + across the endodermis, and then increases the root-to-shoot delivery of Na + via transpiration flow, thereby leading to a transpiration-dependent salt hypersensitivity. Moreover, we show that the ortholog of ZmESBL also mediates CS development and TDST in Arabidopsis. Our study suggests that modification of CS barrier may provide an approach for developing salt-tolerant crops.