Natural variation of an EF-hand Ca(2+)-binding-protein coding gene confers saline-alkaline tolerance in maize.

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.