Suppr超能文献

细胞周期调控的cdc25C基因无TATA框核心启动子的特征分析

Characterization of the TATA-less core promoter of the cell cycle-regulated cdc25C gene.

作者信息

Körner K, Wolfraim L A, Lucibello F C, Müller R

机构信息

Institut für Molekularbiologie und Tumorforschung (IMT), Philipps-Universität Marburg, Emil-Mannkopff-Strasse 2, D-35033 Marburg, Germany.

出版信息

Nucleic Acids Res. 1997 Dec 15;25(24):4933-9. doi: 10.1093/nar/25.24.4933.

Abstract

The TATA- and Inr-less promoter of the human cdc25C gene is regulated during the cell cycle through binding of a repressor to two contiguous promoter-proximal elements, the CDE and CHR. In this study we have characterized in detail the region of the cdc25C promoter immediately downstream of these elements. Several lines of evidence suggest that this region of approximately 60 bp acts as the core promoter. This sequence: (i) harbors most of the transcription initiation sites; (ii) possesses basal promoter activity in vivo ; (iii) shows no stable protein binding in vivo as indicated by genomic dimethyl sulfate and phenanthroline copper footprinting; (iv) contains single-stranded regions in vivo as shown by potassium permanganate footprinting; (v) is hypersensitive to DNase I cleavage in permeabilized cells. Mutational analysis of the core promoter revealed the presence of three sites which play a role in transcription. Two of these sites were found to represent low affinity binding sites for transcription factors of the Sp1 family. Mutation of these sites led to decreased levels of transcription, while their alteration to canonical Sp1 sites impaired cell cycle regulation. Thus the transient interaction of Sp1 with the core promoter appears to be necessary for maximal transcription without perturbing cell cycle regulation.

摘要

人类cdc25C基因的无TATA盒和起始子元件的启动子在细胞周期中通过一种阻遏物与两个相邻的启动子近端元件CDE和CHR结合而受到调控。在本研究中,我们详细表征了cdc25C启动子中紧接这些元件下游的区域。多条证据表明,这个约60 bp的区域充当核心启动子。该序列:(i) 包含大部分转录起始位点;(ii) 在体内具有基础启动子活性;(iii) 如基因组硫酸二甲酯和菲咯啉铜足迹法所示,在体内未显示稳定的蛋白质结合;(iv) 如高锰酸钾足迹法所示,在体内含有单链区域;(v) 对通透细胞中的DNase I切割高度敏感。核心启动子的突变分析揭示了三个在转录中起作用的位点。其中两个位点被发现代表Sp1家族转录因子的低亲和力结合位点。这些位点的突变导致转录水平降低,而将它们改变为典型的Sp1位点则损害细胞周期调控。因此,Sp1与核心启动子的瞬时相互作用似乎是实现最大转录而不干扰细胞周期调控所必需的。

相似文献

本文引用的文献

5
Cell cycle regulation of E2F site occupation in vivo.体内E2F位点占据的细胞周期调控
Science. 1996 Mar 15;271(5255):1595-7. doi: 10.1126/science.271.5255.1595.

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