The roles of clock components in salt stress tolerance remain incompletely characterized in rice. Here, we show that, among OsPRR (Oryza sativa Pseudo‐Response Regulator) family members, OsPRR73 specifically confers salt tolerance in rice. Notably, the grain size and yield of osprr73 null mutants were significantly decreased in the presence of salt stress, with accumulated higher level of reactive oxygen species and sodium ions. RNA sequencing and biochemical assays identified OsHKT2;1, encoding a plasma membrane‐localized Na⁺ transporter, as a transcriptional target of OsPRR73 in mediating salt tolerance. Correspondingly, null mutants of OsHKT2;1 displayed an increased tolerance to salt stress. Immunoprecipitation‐mass spectrometry (IP‐MS) assays further identified HDAC10 as nuclear interactor of OsPRR73 and co‐repressor of OsHKT2;1. Consistently, H3K9ac histone marks at OsHKT2;1 promoter regions were significantly reduced in osprr73 mutant. Together, our findings reveal that salt‐induced OsPRR73 expression confers salt tolerance by recruiting HDAC10 to transcriptionally repress OsHKT2;1, thus reducing cellular Na⁺ accumulation. This exemplifies a new molecular link between clock components and salt stress tolerance in rice.

中文翻译：

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时钟组件 OsPRR73 通过调节 OsHKT2;1 介导的钠稳态来正向调节水稻耐盐性


水稻时钟成分在耐盐胁迫中的作用仍未完全表征。在这里，我们发现，在OsPRR （ Oryza sativa Pseudo-Response Regulator ）家族成员中， OsPRR73特别赋予水稻耐盐性。值得注意的是，在盐胁迫下， osprr73无效突变体的晶粒尺寸和产量显着降低，活性氧和钠离子的积累水平更高。 RNA测序和生化测定鉴定出OsHKT2;1 ，编码质膜定位的Na ⁺转运蛋白，作为OsPRR73介导耐盐性的转录靶标。相应地， OsHKT2;1的无效突变体表现出对盐胁迫的耐受性增加。免疫沉淀-质谱 (IP-MS) 分析进一步鉴定 HDAC10 是 OsPRR73 的核相互作用蛋白和OsHKT2 的共阻遏蛋白；1 。一致地， OsHKT2;1启动子区域的 H3K9ac 组蛋白标记在osprr73突变体中显着减少。总之，我们的研究结果表明，盐诱导的OsPRR73表达通过招募 HDAC10 转录抑制OsHKT2;1来赋予盐耐受性，从而减少细胞 Na ⁺积累。这例证了水稻时钟成分与耐盐胁迫性之间的新分子联系。