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