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.

灌溉土地日益盐化，这对农业生产力产生了不利影响。为了应对高钠 (Na ⁺ ) 浓度，植物拥有多个 Na ⁺运输系统。水稻 ( Oryza sativa ) 高亲和力钾 (K ⁺ ) 转运蛋白 1;5 (OsHKT1;5) 是一种 Na ⁺选择性转运蛋白，在盐胁迫下维持 K ⁺ /Na ⁺稳态。然而，调节OsHKT1;5表达的机制仍不清楚。在这里，我们提出了由水稻 BCL-2 相关 ATHANOGENE4 (OsBAG4)、OsMYB106 和 OsSUVH7 组成的蛋白质复合物调节OsHKT1;5表达以响应盐胁迫的证据。我们分离出一个盐胁迫敏感突变体osbag4-1 ，其显示芽中OsHKT1;5表达显着降低，K ^{+ 水平}降低，Na ⁺水平升高。通过比较相互作用组学，我们分离了两种 OsBAG4 相互作用蛋白，OsMYB106（一种 MYB 转录因子）和 OsSUVH7（一种 DNA 甲基化阅读器），它们对于OsHKT1;5 的表达至关重要。 OsMYB106 和 OsSUVH7 分别与OsHKT1;5启动子中的 MYB 结合顺式元件 (MYBE) 和 MYBE 上游的微型反向重复转座元件 (MITE) 结合。 OsBAG4 作为 OsSUVH7 和 OsMYB106 之间的桥梁，促进 OsMYB106 与OsHKT1;5启动子中的共有 MYBE 结合，从而激活OsHKT1;5表达。消除 MITE 或敲除OsMYB106或OsSUVH7会降低OsHKT1;5 的表达并增加盐敏感性。 我们的研究结果揭示了一个转录复合物，由 DNA 甲基化阅读器、分子伴侣调节剂和转录因子组成，在盐度胁迫期间协同调节OsHKT1;5 的表达。