Summary In Arabidopsis, the high‐affinity K+ transporter HAK5 is the major pathway for root K+ uptake when below 100 µM; HAK5 responds to Low‐K+ (LK) stress by strongly and rapidly increasing its expression during K+‐deficiency. Therefore, positive regulators of HAK5 expression have the potential to improve K+ uptake under LK. Here, we show that mutants of the transcription factor MYB77 share a LK‐induced leaf chlorosis phenotype, lower K+ content, and lower Rb+ uptake of the hak5 mutant, but not the shorter root growth, and that overexpression of MYB77 enhanced K+ uptake and improved tolerance to LK stress. Furthermore, we demonstrated that MYB77 positively regulates the expression of HAK5, by binding to the HAK5 promoter and enhances high‐affinity K+ uptake of roots. As such, our results reveal a novel pathway for enhancing HAK5 expression under LK stress, and provides a candidate for increasing the tolerance of plants to LK.

RAV transcription factors (TFs) are unique to higher plants and contain both B3 and APETALA2 (AP2) DNA binding domains. Although sets of RAV genes have been identified from several species, little is known about this family in wheat. In this study, 26 RAV genes were identified in the wheat genome. These wheat RAV TFs were phylogenetically clustered into three classes based on their amino acid sequences. A TaRAV gene located on chromosome 1D was cloned and named TaRAV1. TaRAV1 was expressed in roots, stems, leaves, and inflorescences, and its expression was up-regulated by heat while down-regulated by salt, ABA, and GA. Subcellular localization analysis revealed that the TaRAV1 protein was localized in the nucleus. The TaRAV1 protein showed DNA binding activity in the EMSA assay and transcriptional activation activity in yeast cells. Overexpressing TaRAV1 enhanced the salt tolerance of Arabidopsis and upregulated the expression of SOS genes and other stress response genes. Collectively, our data suggest that TaRAV1 functions as a transcription factor and is involved in the salt stress response by regulating gene expression in the SOS pathway.