Single‐gene mutants tolerant or sensitive to salt stress are ideal materials for identifying and cloning genes related to salt tolerance in rice (Oryza sativa L.). In the present study, a salt‐sensitive mutant was obtained from the ethyl methanesulfonate (EMS)‐induced Nipponbare bank. The mutant, designated rice salt sensitive 4 (rss4), showed a significant increase in salt sensitivity at the seedling stage and accumulated high levels of Na+ in shoots, particularly in the blades of old leaves, under conditions of NaCl stress. Genetic analysis indicated that the mutation was controlled by a single recessive gene. Quantitative trait locus (QTL) analysis for shoot Na+ content was performed using an F2 population derived from a cross between the rss4 mutant and the indica cultivar Zhaiyeqing 8 (ZYQ8). Three QTLs were identified and one located on the long arm of chromosome 6 was determined to be the candidate locus of the rss4 gene based on comparison and analysis, which explained 40.5% of the phenotypic variance in the shoot Na+ content of the F2 population. Further analysis of recombination events in 165 mutant individuals of an enlarged mapping population of rss4/ZYQ8 defined the rss4 locus to an interval of 230.5 kb bracketed by markers RM20566 and IM28706 on chromosome 6.
Salt-tolerant mutants are valuable resources for basic and applied research on plant salt tolerance. Here, we report the isolation and characterisation of a salt-tolerant rice (Oryza sativa L.) mutant. This mutant was identified from an ethyl methanesulfonate-induced Nipponbare mutant library, designated as rice salt tolerant 1 (rst1). The rst1 mutant was tolerant to salt stress and showed significantly higher shoot biomass and chlorophyll content, but lower lipid peroxidation and electrolyte leakage under NaCl stress. The improved salt tolerance of this mutant may be due mainly to its enhanced ability to restrict Na+ accumulation in shoots under salt stress conditions. Genetic analysis indicated that the salt tolerance of the rst1 mutant was controlled by a single recessive gene. Quantitative trait locus (QTL) mapping for salt tolerance was performed using an F2 population of rst1 × Peiai 64. Two QTLs were detected, in which the locus on chromosome 6 was determined to be the candidate locus of the rst1 gene. The rst1 locus was subsequently shown to reside within a 270.4-kb region defined by the markers IM29432 and IM29702. This result will be useful for map-based cloning of the rst1 gene and for marker-assisted breeding for salt tolerance in rice.
Salt stress impairs nutrient metabolism in plant cells, leading to growth and yield penalties. However, the mechanism by which plants alter their nutrient metabolism processes in response to salt stress remains elusive. 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. Map-based cloning revealed that the gene
RST1
encoded an auxin response factor (OsARF18). Molecular analyses showed that RST1 directly repressed the expression of the gene encoding asparagine synthetase 1 (OsAS1). Loss of
RST1
function increased the expression of
OsAS1
and improved nitrogen (N) utilization by promoting asparagine production and avoiding excess ammonium (NH
4
+
) accumulation.
RST1
was undergoing directional selection during domestication. The superior haplotype RST1
Hap III
decreased its transcriptional repression activity and contributed to salt tolerance and grain weight. 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.
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