Suppr超能文献

在非洲爪蟾囊胚后期胚胎中,用TBP结合蛋白Dr1(NC2β)过表达时,II类基因转录受到抑制,而III类和I类基因转录未受抑制。

Inhibition of transcription of class II, but not class III and I, genes in Xenopus postblastular embryos overexpressed with the TBP-binding protein, Dr1 (NC2beta).

作者信息

Nagano M, Shiokawa K

机构信息

Laboratory of Molecular Embryology, Department of Biological Sciences, Graduate School of Science, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.

出版信息

Biochem Biophys Res Commun. 1999 Nov 30;265(3):644-51. doi: 10.1006/bbrc.1999.1722.

Abstract

Dr1 (NC2beta) is known to effectively repress transcription of class II genes, and much less effectively class III genes, but not class I genes through its binding to the TATA-binding protein (TBP), which is the major component of the basal transcription factor for polymerases II, III, and I. Previously, we isolated Xenopus Dr1 cDNA, and demonstrated that its mRNA is transcribed in oocytes and is inherited into early embryos, but its level decreases in later stages. Here, we overexpressed Xenopus Dr1 in Xenopus embryos and, found that the overexpression significantly reduces the levels of poly(A), cytoskeletal actin and histone H4 mRNAs, and the labeling of heterogeneous mRNA-like RNA in postblastular embryos, without affecting tRNA and rRNA syntheses. These results indicate that the overexpressed Dr1 specifically down-regulates the transcription of class II, but not class III and I, genes, and suggest that Dr1 plays an important role in the control of transcription in Xenopus embryogenesis.

摘要

已知Dr1(NC2β)可通过与TATA结合蛋白(TBP)结合有效地抑制II类基因的转录,对III类基因的抑制效果则弱得多,但对I类基因无抑制作用。TBP是聚合酶II、III和I的基础转录因子的主要成分。此前,我们分离出了非洲爪蟾Dr1 cDNA,并证明其mRNA在卵母细胞中转录并遗传至早期胚胎,但在后期其水平会下降。在此,我们在非洲爪蟾胚胎中过表达Dr1,发现过表达显著降低了囊胚后期胚胎中多聚腺苷酸、细胞骨架肌动蛋白和组蛋白H4 mRNA的水平,以及异质mRNA样RNA的标记,而不影响tRNA和rRNA的合成。这些结果表明,过表达的Dr1特异性下调II类基因而非III类和I类基因的转录,并提示Dr1在非洲爪蟾胚胎发育过程中的转录调控中起重要作用。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验