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小鼠Surf-1基因和Surf-2基因反向转录的双向启动子。

The bidirectional promoter of the divergently transcribed mouse Surf-1 and Surf-2 genes.

作者信息

Lennard A C, Fried M

机构信息

Department of Eukaryotic Gene Organization and Expression, Imperial Cancer Research Fund, London, United Kingdom.

出版信息

Mol Cell Biol. 1991 Mar;11(3):1281-94. doi: 10.1128/mcb.11.3.1281-1294.1991.

DOI:10.1128/mcb.11.3.1281-1294.1991
PMID:1996091
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC369399/
Abstract

The ubiquitously expressed mouse Surf-1 and Surf-2 genes are divergently transcribed, and their heterogeneous start sites are separated by up to a maximum of only 73 bp. By using in vitro DNase I, dimethyl sulfate methylation, and gel retardation assays, we have identified five putative promoter control elements between and around the Surf-1 and Surf-2 start sites. The effects of each site on the regulation of Surf-1 and Surf-2 transcription have been studied in vivo, and four sites were found to be functional promoter elements. A novel binding site is required for efficient use of the intermediate but not the major start site of Surf-1. Three elements function in a bidirectional manner and are shared for efficient and accurate expression of both Surf-1 and Surf-2. One is an UEF (USF, MLTF) binding site which had a small effect on the use of the intermediate start sites of Surf-1 and also affected the major start sites of Surf-2. Another has sequence homology to the RPG alpha binding site associated with some ribosomal protein gene promoters and is required for efficient expression of the major but not intermediate start sites of Surf-1 and all start sites of Surf-2. The third, an RPG alpha-like site, is used for all start sites of both Surf-1 and Surf-2. Dissection of this cellular promoter region showed that different binding sites affect the use of different start sites and revealed a complex interaction between multiple elements that constitute a bona fide bidirectional promoter.

摘要

普遍表达的小鼠Surf-1和Surf-2基因呈反向转录,其异质起始位点之间的间隔最大仅为73 bp。通过体外DNase I、硫酸二甲酯甲基化和凝胶阻滞试验,我们在Surf-1和Surf-2起始位点之间及其周围鉴定出五个假定的启动子控制元件。已在体内研究了每个位点对Surf-1和Surf-2转录调控的影响,发现四个位点是功能性启动子元件。Surf-1的中间起始位点(而非主要起始位点)的有效利用需要一个新的结合位点。三个元件以双向方式发挥作用,是Surf-1和Surf-2高效准确表达所共有的。一个是UEF(USF、MLTF)结合位点,对Surf-1中间起始位点的利用影响较小,也影响Surf-2的主要起始位点。另一个与一些核糖体蛋白基因启动子相关的RPGα结合位点具有序列同源性,是Surf-1主要起始位点(而非中间起始位点)和Surf-2所有起始位点高效表达所必需的。第三个是类似RPGα的位点,用于Surf-1和Surf-2的所有起始位点。对该细胞启动子区域的剖析表明,不同的结合位点影响不同起始位点的利用,并揭示了构成真正双向启动子的多个元件之间的复杂相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bdb/369399/61ae23de4baa/molcellb00166-0117-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bdb/369399/b268cd54a63d/molcellb00166-0109-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bdb/369399/2e9b44e6a568/molcellb00166-0112-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bdb/369399/bf2acd0b88cf/molcellb00166-0114-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bdb/369399/df9e733536fa/molcellb00166-0116-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bdb/369399/61ae23de4baa/molcellb00166-0117-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bdb/369399/b268cd54a63d/molcellb00166-0109-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bdb/369399/2e9b44e6a568/molcellb00166-0112-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bdb/369399/bf2acd0b88cf/molcellb00166-0114-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bdb/369399/df9e733536fa/molcellb00166-0116-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bdb/369399/61ae23de4baa/molcellb00166-0117-a.jpg

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