The HaMYB22–HaGST3.2 module mediates salt stress response in sunflower

ABSTRACT Soil salinization is a global challenge threatening agricultural production, food security, and sustainable development. As a pioneer crop on saline‐alkali land, sunflower plays a crucial role in the improvement and utilization of salt‐affected soils. However, the molecular mechanisms underlying sunflower salt tolerance remain poorly understood. In this study, we identified a key R2R3‐MYB gene, HaMYB22 , through a combination of genome and transcriptome analyses. Functional characterization demonstrates that overexpression of HaMYB22 significantly enhances salt tolerance in both Arabidopsis and sunflower, whereas its silencing decreases salt resistance. Protein interaction assays revealed that HaMYB22 interacts with HaMYB120 and HaMYB181. Glutathione S‐transferase HaGST3.2 was identified as a direct target of HaMYB22, and superior haplotype HaMYB22 hap1 can strongly increase HaGST3.2 transcripts. Moreover, HaMYB120 and HaMYB181 synergistically strengthen HaMYB22‐mediated HaGST3.2 activation. HaGST3.2 silencing in sunflower decreases salt tolerance. Our findings revealed the importance of the HaMYB22–HaGST3.2 module in sunflower salt tolerance.