MaMYB102 enhances salt tolerance in banana (Musa acuminata) by activating MaBADH-mediated glycine betaine biosynthesis

Abstract

Salinity is a major abiotic stress that limits banana (Musa acuminata) growth and productivity. Transcription factors play crucial roles in regulating plant stress responses; however, the molecular mechanisms underlying salt tolerance in banana remain largely unexplored. In this study, we identified and functionally characterized MaMYB102, an R2R3-type MYB transcription factor that positively regulates salt tolerance in banana. Subcellular localization analysis confirmed that MaMYB102 is a nuclear protein. Transient overexpression of MaMYB102 in banana leaves enhanced salt tolerance, as evidenced by reduced chlorosis, elevated antioxidant capacity, and decreased hydrogen peroxide (H₂O₂) accumulation under 0.3 M NaCl treatment. Conversely, transient silencing of MaMYB102 increased salt sensitivity and oxidative damage. Yeast one-hybrid (Y1H) and electrophoretic mobility shift assays (EMSA) demonstrated that MaMYB102 binds directly to the promoter region of MaBADH, a key gene involved in glycine betaine (GB) biosynthesis. Dual-luciferase assays further confirmed that MaMYB102 activates MaBADH transcription. Overexpression of MaMYB102 increased MaBADH expression and GB accumulation, whereas silencing MaMYB102 suppressed both. Collectively, our results reveal that MaMYB102 enhances salt tolerance in banana by activating MaBADH-mediated glycine betaine biosynthesis, thereby improving redox homeostasis under saline conditions. This study provides novel insights into the MYB-regulated salt stress response and offers a potential target for developing salt-tolerant banana cultivars.