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人类弹性蛋白酶I基因(ELA1)的进化沉默

Evolutionary silencing of the human elastase I gene (ELA1).

作者信息

Rose S D, MacDonald R J

机构信息

Department of Molecular Biology and Oncology, University of Texas Southwestern Medical Center, Dallas 75235-9140, USA.

出版信息

Hum Mol Genet. 1997 Jun;6(6):897-903. doi: 10.1093/hmg/6.6.897.

Abstract

The human pancreatic elastase I gene is transcriptionally silent, despite the apparent integrity of the structural gene. The transcriptional regulatory sequences necessary and sufficient for transcription of the active rat homologue are localized within 205 base pairs (bp) of the transcriptional start and comprise a pancreas-specific transcriptional enhancer of 134 bp immediately upstream of a 71 bp non-specific promoter. The human gene has 58 nucleotide differences within this region, 13 of which are in the three functional elements (A, B and C) that constitute the enhancer. Through cell transfection analyses with a pancreatic acinar tumor cell line, we show that the nucleotide differences in the human 5' flanking gene sequences have inactivated both the enhancer and the promoter. The changes in the three elements of the human enhancer alone are sufficient to inactivate the enhancer; conversely, restoring these to the rat configuration partially restores the activity of the human enhancer. The two mutations in the A element and the four mutations in the B element abolish the binding of the transcription factors previously shown to mediate the activity of these elements. Replacing the active 71 bp rat promoter with the human promoter also prevents expression. Therefore, the evolutionary silencing of the human elastase I gene appears due to mutations that inactivate crucial enhancer and promoter elements.

摘要

尽管人类胰腺弹性蛋白酶I基因的结构基因看似完整,但其转录是沉默的。活性大鼠同源基因转录所必需且充分的转录调控序列位于转录起始点的205个碱基对(bp)范围内,包括一个134 bp的胰腺特异性转录增强子,紧邻一个71 bp的非特异性启动子上游。人类基因在该区域内有58个核苷酸差异,其中13个位于构成增强子的三个功能元件(A、B和C)中。通过对胰腺腺泡肿瘤细胞系进行细胞转染分析,我们发现人类5'侧翼基因序列中的核苷酸差异使增强子和启动子均失活。仅人类增强子的三个元件发生变化就足以使增强子失活;相反,将这些元件恢复为大鼠的构型可部分恢复人类增强子的活性。A元件中的两个突变和B元件中的四个突变消除了先前显示介导这些元件活性的转录因子的结合。用人类启动子取代活性71 bp的大鼠启动子也会阻止表达。因此,人类弹性蛋白酶I基因的进化沉默似乎是由于使关键增强子和启动子元件失活的突变所致。

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