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.

Highlights

  • Sodium (Na+) toxicity is one of the major damages imposed on crops by saline-alkaline stress

  • Since the major feature distinguishing saline-alkaline stress from saline stress is the high pH stress, we suggest that high pH stress boosts maize shoot Na+ accumulation under high-Na+ conditions

  • While the growth of wild type and ZmNSA1overexpressing plants were comparable under control condition, ZmNSA1oe-1 and ZmNSA1oe-2 plants were significantly smaller and conferred greater shoot Na+ contents than wild type under NaHCO3 condition (Fig. 2i–k). These results indicated that ZmNSA1 is associated with shoot Na+ content and saline-alkaline (NaHCO3) tolerance, supporting the perspective that GRMZM2G000397 is the candidate of ZmNSA1

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Summary

Introduction

Sodium (Na+) toxicity is one of the major damages imposed on crops by saline-alkaline stress. The H+ efflux from root to soil acidifies the rhizosphere promotes adaptation to high pH stress[6], the Na+-preferring transporters (e.g., SOS1 and HKT1) enable the circumvention of Na+ toxicity[2,7], the accumulation of osmoprotectants (e.g., glycinebetaine) attenuates osmotic damage[8]. These adaptive mechanisms act together to enable plant to survive saline-alkaline stress. These observations indicate that the transcriptional regulation of PM-H+-ATPase is important for the regulation of root H+ efflux under stress conditions, the mechanism remains largely unknown

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