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时钟元件 OsPRR73 通过调节 OsHKT2;1 介导的钠离子稳态正向调控水稻的耐盐性。

Clock component OsPRR73 positively regulates rice salt tolerance by modulating OsHKT2;1-mediated sodium homeostasis.

机构信息

Key Laboratory of Plant Molecular Physiology, CAS Center for Excellence in Molecular Plant Sciences, Institute of Botany, Chinese Academy of Sciences, Beijing, China.

University of Chinese Academy of Sciences, Beijing, China.

出版信息

EMBO J. 2021 Feb 1;40(3):e105086. doi: 10.15252/embj.2020105086. Epub 2020 Dec 21.

DOI:10.15252/embj.2020105086
PMID:33347628
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7849171/
Abstract

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.

摘要

在水稻中,时钟组件在耐盐性中的作用仍不完全清楚。在这里,我们表明,在 OsPRR(水稻拟南芥假应答调节剂)家族成员中,OsPRR73 特异性赋予水稻耐盐性。值得注意的是,在盐胁迫下,osprr73 缺失突变体的粒大小和产量显著降低,积累了更高水平的活性氧和钠离子。RNA 测序和生化分析鉴定出 OsHKT2;1,编码一种质膜定位的 Na 转运体,是 OsPRR73 介导耐盐性的转录靶标。相应地,OsHKT2;1 的缺失突变体对盐胁迫表现出更高的耐受性。免疫沉淀-质谱(IP-MS)分析进一步鉴定出 HDAC10 是 OsPRR73 的核相互作用因子和 OsHKT2;1 的共阻遏物。一致地,osprr73 突变体中 OsHKT2;1 启动子区域的 H3K9ac 组蛋白标记显著减少。总之,我们的研究结果表明,盐诱导的 OsPRR73 表达通过招募 HDAC10 来转录抑制 OsHKT2;1,从而减少细胞内 Na 积累,赋予水稻耐盐性。这例证了水稻中时钟组件与耐盐性之间的新的分子联系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/7849171/7e22aa3a3cad/EMBJ-40-e105086-g014.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/7849171/124f1c66f4d3/EMBJ-40-e105086-g012.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/7849171/c70387b8a3d2/EMBJ-40-e105086-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/7849171/5c2882aee282/EMBJ-40-e105086-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/7849171/124f1c66f4d3/EMBJ-40-e105086-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/7849171/fb6301776762/EMBJ-40-e105086-g013.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/7849171/9a31369a3f05/EMBJ-40-e105086-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/629a/7849171/7e22aa3a3cad/EMBJ-40-e105086-g014.jpg

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