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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.

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