稻米中时钟成分在耐盐胁迫中的作用仍未完全清楚。本研究表明，在OsPRR（水稻伪响应调节剂）家族成员中，OsPRR73特别赋予水稻耐盐性。 值得注意的是，在存在盐胁迫的情况下，osprr73无义突变体的籽粒大小和产量显着降低，并且活性氧和钠离子积累水平较高。
RNA测序和生化分析确定了编码质膜定位的Na +转运蛋白的OsHKT2; 1作为OsPRR73介导耐盐性的转录靶标。 相应地，OsHKT2; 1的无义突变体显示出对盐胁迫的增加的耐受性。
免疫沉淀质谱（IP-MS）分析进一步确定HDAC10是OsPRR73的核相互作用体和OsHKT2的共阻遏物； osprr73突变体中OsHKT2; 1启动子区域的H3K9ac组蛋白标记显着减少。
综上我们的发现揭示了盐诱导的OsPRR73表达通过募集HDAC10转录抑制OsHKT2; 1，从而减少了细胞中Na +的积累，从而赋予了盐耐受性。
这体现稻米中时钟成分和耐盐性之间存在新分子联系。
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.
https://www.embopress.org/doi/epdf/10.15252/embj.2020105086
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