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OsHDA710-Mediated Histone Deacetylation Regulates Callus Formation of Rice Mature Embryo.
Plant & Cell Physiology ( IF 4.9 ) Pub Date : 2020-06-27 , DOI: 10.1093/pcp/pcaa086
Haidao Zhang 1 , Fu Guo 1 , Peipei Qi 1 , Yizi Huang 1 , Yongyao Xie 2 , Lei Xu 3 , Ning Han 1 , Lin Xu 4 , Hongwu Bian 1
Affiliation  

Histone deacetylases (HDACs) play important roles in the regulation of eukaryotic gene expression. The role of HDACs in specialized transcriptional regulation and biological processes is poorly understood. In this study, we evaluated the global expression patterns of genes related to epigenetic modifications during callus initiation in rice. We found that the repression of HDAC activity by trichostatin A (TSA) or by OsHDA710 mutation (hda710) results in impaired callus formation of rice mature embryo and increased global histone H3 acetylation levels. The HDAC inhibition decreased auxin response and cell proliferation in callus formation. Meanwhile, the transcriptional repressors OsARF18 and OsARF22 were upregulated in the callus of hda710. The chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR) analysis demonstrated that the callus of hda710 exhibited enhanced histone H3 acetylation levels at the chromatin regions of OsARF18 and OsARF22. Furthermore, we found that OsARF18 and OsARF22 were regulated through OsHDA710 recruitment to their target loci. In addition, overexpression of OsARF18 decreased the transcription of downstream genes PLT1 and PLT2 and inhibited callus formation of the mature embryo. These results demonstrate that OsHDA710 regulates callus formation by suppressing repressive OsARFs via histone deacetylation during callus formation of rice mature embryo. This indicates that OsHDA710-mediated histone deacetylation is an epigenetic regulation pathway for maintaining auxin response during cell dedifferentiation.

中文翻译:

OsHDA710介导的组蛋白去乙酰化调节水稻成熟胚的愈伤组织形成。

组蛋白脱乙酰基酶(HDACs)在真核基因表达的调节中起重要作用。HDAC在专门的转录调控和生物学过程中的作用了解甚少。在这项研究中,我们评估了水稻愈伤组织起始过程中与表观遗传修饰相关的基因的整体表达模式。我们发现,曲古抑菌素A(TSA)或OsHDA710突变(hda710)抑制HDAC活性会导致水稻成熟胚的愈伤组织形成受损,并增加整体组蛋白H3乙酰化水平。HDAC抑制降低了愈伤组织形成中的生长素应答和细胞增殖。同时,转录抑制基因OsARF18OsARF22在愈伤组织中被上调。hda710。染色质免疫沉淀定量PCR(ChIP-qPCR)分析表明,hda710的愈伤组织在OsARF18OsARF22的染色质区域表现出增强的组蛋白H3乙酰化水平。此外,我们发现OsARF18OsARF22通过OsHDA710募集到其目标基因座而受到调控。此外,过表达OsARF18下游基因的转录降低PLT1PLT2和抑制愈伤组织形成成熟胚的。这些结果表明,OsHDA710通过抑制抑制性OsARF来调节愈伤组织的形成。水稻成熟胚愈伤组织形成过程中通过组蛋白脱乙酰作用。这表明OsHDA710介导的组蛋白去乙酰化是在细胞去分化过程中维持生长素反应的表观遗传调控途径。
更新日期:2020-06-27
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