背景回顾：Salt stress impairs nutrient metabolism in plant cells, leading to growth and yield penalties. 

提出问题：However, the mechanism by which plants alter their nutrient metabolism processes in response to salt stress remains elusive.

主要发现：In this study, we identified and characterized the rice (Oryza sativa) rice salt tolerant 1 (rst1) mutant, which displayed improved salt tolerance and grain yield. 

结果1-RST1基因克隆：Map-based cloning revealed that the gene RST1 encoded an auxin response factor (OsARF18). 

结果2-RST1下游靶基因：Molecular analyses showed that RST1 directly repressed the expression of the gene encoding asparagine synthetase 1 (OsAS1). 

结果3-RST1-OsAS1-氮利用：Loss of RST1 function increased the expression of OsAS1 and improved nitrogen (N) utilization by promoting asparagine production and avoiding excess ammonium (NH4+) accumulation. 

结果4-RST1演化：RST1 was undergoing directional selection during domestication. The superior haplotype RST1Hap III decreased its transcriptional repression activity and contributed to salt tolerance and grain weight. 

结论：Together, our findings unravel a synergistic regulator of growth and salt tolerance associated with N metabolism and provide a new strategy for the development of tolerant cultivars.

A proposed working model of RST1 in the regulation of rice growth and salt tolerance.

盐胁迫损伤植物细胞中的营养代谢，从而导致其在生长和产量上的损失。但是， 植物在响应于盐胁迫，通过什么样的机制来改变自身的营养代谢还不清楚。本文中，作者鉴定到了一个水稻耐盐突变体rst1，其表现出盐耐受性和籽粒产量增强的表型。图位克隆表明RST1基因编码一个生长素响应因子OsARF18。分子分析显示，RST1直接抑制天冬酰胺合成酶OsAS1编码基因的表达。RST1功能缺失突变会导致OsAS1表达的增强，从而通过促进天冬氨酸的产量和避免过量铵根离子的积累提升植物对氮的利用。RST1基因在驯化过程中受到了直接选择。RST1 Hap III单倍型降低了自身的转录抑制活性，从而作用于盐耐受性和籽粒产量的提升。综上，本文的研究结果揭示了一个与氮代谢相关的生长和盐耐受性协同调控子，为未来培育耐盐性栽培种提供一个新的策略。

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