Natural variation of an EF-hand Ca²⁺-binding-protein coding gene confers saline-alkaline tolerance in maize.

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 (NaHCO₃) tolerance, and reveal that ZmNSA1 (Na⁺ Content under Saline-Alkaline Condition) confers shoot Na⁺ variations under NaHCO₃ 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, Ca²⁺ 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 Ca²⁺-triggered saline-alkaline tolerance and provide an important gene target for breeding saline-alkaline tolerant maize varieties.