TaGW2-TaVOZ1 module regulates wheat salt tolerance via both E3 ligase-dependent and -independent pathways.

Abstract

Wheat production is limited by the rapid expansion of salinized arable land worldwide. Identification of the molecular mechanisms that underlie the salt stress response is of great importance. Here, we uncovered the NAC-type transcription factor, TaVOZ1, as a positive regulator of wheat salt tolerance. Its overexpression could enhance yield and biomass production under salt stress, while <i>TaVOZ1</i> knockdown attenuates salt tolerance. TaVOZ1 transcriptionally activates stress-responsive genes, especially <i>HKT1</i>-family transporters, decreasing shoot Na⁺ accumulation. However, the RING-type E3 ligase, TaGW2, directly interacts with and ubiquitinates TaVOZ1, promoting its ubiquitin/26<i>S</i> proteasomal degradation. <i>TaGW2</i> overexpression reduces salt tolerance, while its knockdown or knockout enhances wheat response to salt stress. Moreover, we found a moonlight function of TaGW2 wherein it binds the same DNA motifs as TaVOZ1 to block its up-regulation of <i>HKT1</i>-family genes while coordinately governing both the salt tolerance and grain yield. This study highlights the functional versatility of TaGW2 and defines an antagonistic TaGW2-TaVOZ1 regulatory module in wheat salt tolerance.