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I 类和 II 类 RPD3 样组蛋白去乙酰化酶在盐胁迫响应中的独特作用。

The Distinct Roles of Class I and II RPD3-Like Histone Deacetylases in Salinity Stress Response.

机构信息

Plant Genomic Network Research Team, RIKEN Center for Sustainable Resource Science, Yokohama, Kanagawa 230-0045, Japan.

Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Kawaguchi, Saitama 332-0012, Japan.

出版信息

Plant Physiol. 2017 Dec;175(4):1760-1773. doi: 10.1104/pp.17.01332. Epub 2017 Oct 10.

DOI:10.1104/pp.17.01332
PMID:29018096
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5717743/
Abstract

Histone acetylation is an essential process in the epigenetic regulation of diverse biological processes, including environmental stress responses in plants. Previously, our research group identified a histone deacetylase (HDAC) inhibitor (HDI) that confers salt tolerance in Arabidopsis (). In this study, we demonstrate that class I HDAC (HDA19) and class II HDACs (HDA5/14/15/18) control responses to salt stress through different pathways. The screening of 12 different selective HDIs indicated that seven newly reported HDIs enhance salt tolerance. Genetic analysis, based on a pharmacological study, identified which HDACs function in salinity stress tolerance. In the wild-type Columbia-0 background, plants exhibit tolerance to high-salinity stress, while plants exhibit hypersensitivity to salt stress. Transcriptome analysis revealed that the effect of deficiency on the response to salinity stress is distinct from that of deficiencies. In plants, the expression levels of stress tolerance-related genes, late embryogenesis abundant proteins that prevent protein aggregation and positive regulators such as ABI5 and NAC019 in abscisic acid signaling, were induced strongly relative to the wild type. Neither of these elements was up-regulated in the plants. The mutagenesis of HDA19 by genome editing in the plants enhanced salt tolerance, suggesting that suppression of HDA19 masks the phenotype caused by the suppression of class II HDACs in the salinity stress response. Collectively, our results demonstrate that HDIs that inhibit class I HDACs allow the rescue of plants from salinity stress regardless of their selectivity, and they provide insight into the hierarchal regulation of environmental stress responses through HDAC isoforms.

摘要

组蛋白乙酰化是表观遗传调控多种生物学过程的一个必要过程,包括植物的环境胁迫反应。以前,我们的研究小组鉴定出一种组蛋白去乙酰化酶(HDAC)抑制剂(HDI),它赋予拟南芥耐盐性()。在这项研究中,我们证明了 I 类 HDAC(HDA19)和 II 类 HDAC(HDA5/14/15/18)通过不同的途径控制对盐胁迫的反应。对 12 种不同选择性 HDIs 的筛选表明,有 7 种新报道的 HDIs 增强了耐盐性。基于药理学研究的遗传分析确定了哪些 HDACs在盐胁迫耐受性中起作用。在野生型哥伦比亚-0 背景下, 植物表现出对高盐胁迫的耐受性,而 植物对盐胁迫表现出超敏性。转录组分析表明, 缺乏对盐胁迫反应的影响与 缺乏的影响不同。在 植物中,与野生型相比,应激耐受相关基因、防止蛋白质聚集的晚期胚胎丰富蛋白、脱落酸信号中的正调控因子如 ABI5 和 NAC019 的表达水平被强烈诱导。这些元素在 植物中都没有上调。通过基因组编辑对 植物中的 HDA19 进行诱变增强了耐盐性,这表明抑制 HDA19 掩盖了在盐胁迫反应中抑制 II 类 HDAC 所导致的表型。总的来说,我们的结果表明,抑制 I 类 HDAC 的 HDIs 允许植物从盐胁迫中恢复,而不管它们的选择性如何,它们为通过 HDAC 同工型对环境胁迫反应的层次调节提供了见解。