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磷酸烯醇式丙酮酸羧激酶基因启动子中基础和环磷酸腺苷调节元件的鉴定

Identification of basal and cyclic AMP regulatory elements in the promoter of the phosphoenolpyruvate carboxykinase gene.

作者信息

Quinn P G, Wong T W, Magnuson M A, Shabb J B, Granner D K

机构信息

Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee 37232.

出版信息

Mol Cell Biol. 1988 Aug;8(8):3467-75. doi: 10.1128/mcb.8.8.3467-3475.1988.

Abstract

Promoter elements important for basal and cyclic AMP (cAMP)-regulated expression of the phosphoenolpyruvate carboxykinase (PEPCK) gene have been identified by analysis of a series of PEPCK promoter mutations in transfection experiments. Fusion genes containing wild-type and mutated PEPCK promoter sequences from -600 to +69 base pairs (bp) fused to the coding sequence for chloramphenicol acetyltransferase were studied. Internal deletion mutations that replaced specific bases with a 10-bp linker within the region from -129 bp to -18 bp of the PEPCK promoter were examined. In addition, wild-type and mutated DNA templates were used as probes in DNase I protection experiments to determine sites of protein-DNA interaction. The PEPCK promoter contains a binding site for nuclear factor 1-CAAT. Deletion of the 5' end of this binding site reduced the size of the DNase I footprint in this region but had no effect on promoter activity. In contrast, deletion or disruption of the 3' end of this binding site completely eliminated protein binding and reduced promoter activity by 50%. Deletion of core sequences of the cAMP regulatory element (CRE) resulted in loss of cAMP responsiveness and an 85% decrease in basal promoter activity, indicating that the CRE also functions as a basal stimulatory element. Mutation of the core sequence of the CRE resulted in loss of the DNase I footprint over the CRE. Internal deletions flanking the CRE showed no loss of induction by cAMP but did have reduced promoter activity. This delimits the CRE to an 18-bp region between nucleotides -100 and -82. Analysis of mutations that disrupted bases between the CRE and the initiation site identified a basal inhibitory element adjacent to a basal stimulatory element, both located just 3' of the CRE, as well as a basal stimulatory element coincident with the TATA consensus sequence centered at -27. These data demonstrate that several cis-acting elements are located within 130 nucleotides of the initiation site of the PEPCK gene and that the CRE is essential for both basal promoter activity and cAMP-regulated expression of this gene.

摘要

通过在转染实验中对一系列磷酸烯醇式丙酮酸羧激酶(PEPCK)启动子突变进行分析,已确定了对PEPCK基因基础表达和环磷酸腺苷(cAMP)调节表达至关重要的启动子元件。研究了含有从 -600至 +69碱基对(bp)的野生型和突变型PEPCK启动子序列与氯霉素乙酰转移酶编码序列融合的融合基因。检测了在PEPCK启动子 -129 bp至 -18 bp区域内用10 bp接头取代特定碱基的内部缺失突变。此外,野生型和突变型DNA模板在DNase I保护实验中用作探针,以确定蛋白质 - DNA相互作用位点。PEPCK启动子含有一个核因子1 - CAAT的结合位点。该结合位点5'端的缺失减小了该区域DNase I足迹的大小,但对启动子活性没有影响。相反,该结合位点3'端的缺失或破坏完全消除了蛋白质结合,并使启动子活性降低了50%。cAMP调节元件(CRE)核心序列的缺失导致cAMP反应性丧失,基础启动子活性降低85%,表明CRE也作为基础刺激元件发挥作用。CRE核心序列的突变导致CRE上DNase I足迹的丧失。CRE侧翼的内部缺失显示cAMP诱导没有丧失,但启动子活性降低。这将CRE界定为核苷酸 -100和 -82之间的18 bp区域。对破坏CRE和起始位点之间碱基的突变进行分析,确定了一个与基础刺激元件相邻的基础抑制元件,两者都位于CRE的3'端,以及一个与以 -27为中心的TATA共有序列重合的基础刺激元件。这些数据表明,几个顺式作用元件位于PEPCK基因起始位点的130个核苷酸内,并且CRE对于该基因的基础启动子活性和cAMP调节表达都是必不可少的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e781/363584/33e77044c637/molcellb00068-0494-a.jpg

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