A DNA Methylation Reader–Chaperone Regulator–Transcription Factor Complex Activates OsHKT1;5 Expression during Salinity Stress

Abstract

Irrigated lands are increasingly salinized, which adversely affects agricultural productivity. To respond to high sodium (Na⁺) concentrations, plants harbor multiple Na⁺ transport systems. Rice (Oryza sativa) HIGH-AFFINITY POTASSIUM (K⁺) TRANSPORTER1;5 (OsHKT1;5), a Na⁺-selective transporter, maintains K⁺/Na⁺ homeostasis under salt stress. However, the mechanism regulating OsHKT1;5 expression remains unknown. Here, we present evidence that a protein complex consisting of rice BCL-2-ASSOCIATED ATHANOGENE4 (OsBAG4), OsMYB106, and OsSUVH7 regulates OsHKT1;5 expression in response to salt stress. We isolated a salt stress–sensitive mutant, osbag4-1, that showed significantly reduced OsHKT1;5 expression and reduced K⁺ and elevated Na⁺ levels in shoots. Using comparative interactomics, we isolated two OsBAG4-interacting proteins, OsMYB106 (a MYB transcription factor) and OsSUVH7 (a DNA methylation reader), that were crucial for OsHKT1;5 expression. OsMYB106 and OsSUVH7 bound to the MYB binding cis-element (MYBE) and the miniature inverted-repeat transposable element (MITE) upstream of the MYBE, respectively, in the OsHKT1;5 promoter. OsBAG4 functioned as a bridge between OsSUVH7 and OsMYB106 to facilitate OsMYB106 binding to the consensus MYBE in the OsHKT1;5 promoter, thereby activating the OsHKT1;5 expression. Elimination of the MITE or knockout of OsMYB106 or OsSUVH7 decreased OsHKT1;5 expression and increased salt sensitivity. Our findings reveal a transcriptional complex, consisting of a DNA methylation reader, a chaperone regulator, and a transcription factor, that collaboratively regulate OsHKT1;5 expression during salinity stress.