Domestication of Tartary Buckwheat Shaped a Regulatory Module for Seedling Salt Tolerance by Targeting the Magnesium Transporter Gene FtMGT2

Domestication of Tartary buckwheat is selected for a salt tolerance mechanism involving the magnesium transporter FtMGT2. Its expression is controlled by the FtAGL16‐FtMYB15L module, which is stabilized under salt stress through a competitive interaction that blocks its degradation by the E3 ligase FtBRG1, ultimately boosting Na⁺ efflux and plant resilience. Abstract Globally, soil salinization increasingly affects farmland, severely limiting the production of Tartary buckwheat (Fagopyrum tataricum). To identify genetic factors for salt tolerance, we analyzed core Tartary buckwheat accessions and utilized differential expression analysis and genome‐wide association studies (GWAS), identifying a key domesticated magnesium transporter protein, FtMGT2. A single nucleotide polymorphism (SNP) genotype (G/A) of a natural variant located in the FtMGT2 promoter was found to be positively associated with the expression of FtMGT2 and salt tolerance variation. Mechanistically, the MADS transcription factor FtAGL16 binds the A variant more strongly. FtAGL16 and the MYB transcription factor FtMYB15L co‐regulate FtMGT2 transcription, with FtMYB15L protein stability strictly controlled by the E3 ubiquitin ligase FtBRG1. Intriguingly, under salt stress, FtAGL16 can compete with FtBRG1 for binding to FtMYB15L, stabilizing and accumulating FtMYB15L. This enhances FtMGT2 expression, increasing Mg2+ flux, which in turn enhances the transport activity of the sodium (Na+) transporter FtHKT1. This coordinated action leads to increased Na+ efflux and enhanced salt resistance. This study thereby establishes both the theoretical basis and practical application for targeted molecular breeding to enhance plant salt tolerance. Domestication of Tartary buckwheat is selected for a salt tolerance mechanism involving the magnesium transporter FtMGT2. Its expression is controlled by the FtAGL16-FtMYB15L module, which is stabilized under salt stress through a competitive interaction that blocks its degradation by the E3 ligase FtBRG1, ultimately boosting Na⁺ efflux and plant resilience. Abstract Globally, soil salinization increasingly affects farmland, severely limiting the production of Tartary buckwheat ( Fagopyrum tataricum ). To identify genetic factors for salt tolerance, we analyzed core Tartary buckwheat accessions and utilized differential expression analysis and genome-wide association studies (GWAS), identifying a key domesticated magnesium transporter protein, FtMGT2. A single nucleotide polymorphism (SNP) genotype (G/A) of a natural variant located in the FtMGT2 promoter was found to be positively associated with the expression of FtMGT2 and salt tolerance variation. Mechanistically, the MADS transcription factor FtAGL16 binds the A variant more strongly. FtAGL16 and the MYB transcription factor FtMYB15L co-regulate FtMGT2 transcription, with FtMYB15L protein stability strictly controlled by the E3 ubiquitin ligase FtBRG1. Intriguingly, under salt stress, FtAGL16 can compete with FtBRG1 for binding to FtMYB15L, stabilizing and accumulating FtMYB15L. This enhances FtMGT2 expression, increasing Mg 2+ flux, which in turn enhances the transport activity of the sodium (Na + ) transporter FtHKT1. This coordinated action leads to increased Na + efflux and enhanced salt resistance. This study thereby establishes both the theoretical basis and practical application for targeted molecular breeding to enhance plant salt tolerance. Advanced Science, EarlyView.