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控制中国仓鼠卵巢细胞aprt基因表达的信号分析。

Analysis of signals controlling expression of the Chinese hamster ovary aprt gene.

作者信息

Park J H, Taylor M W

机构信息

Department of Biology, Indiana University, Bloomington 47405.

出版信息

Mol Cell Biol. 1988 Jun;8(6):2536-44. doi: 10.1128/mcb.8.6.2536-2544.1988.

Abstract

The 5' end of the Chinese hamster ovary aprt gene was sequenced and transcription start sites were determined by both S1 nuclease protection and primer extension assays. Deletion mutants covering the same area were constructed, and adenine phosphoribosyltransferase (APRT) or chloramphenicol acetyltransferase (CAT) activity was measured by transient-expression assays. The aprt gene uses a single cluster of transcription start sites and lacks consensus sequences such as TATA and CCAAT, which are general components of eucaryotic promoters. The 5' deletion mutations of the promoter sequences demonstrated that (i) there is no decrease in either APRT activity or transcription extending to position -89 (relative to the main transcription start site); (ii) an additional 29-base-pair (bp) deletion decreases APRT activity and transcription twofold; and (iii) a deletion past the transcription start sites (P5' delta +27) abolishes both APRT activity and transcription, indicating that a 60-bp fragment immediately upstream of the main transcription start site is involved in basic transcription and a 29-bp fragment just upstream of the 60 bp-fragment stimulates transcription twofold. The 3' deletion mutations showed that a deletion of a 61-bp fragment in the 5' leader and coding sequence abolishes the efficient translation of an aprt-CAT gene transcript. In addition, there are two polyadenylation signals at the genomic 3' end, with the proximal one being sufficient for functional polyadenylation.

摘要

对中国仓鼠卵巢细胞aprt基因的5'端进行了测序,并通过S1核酸酶保护试验和引物延伸试验确定了转录起始位点。构建了覆盖相同区域的缺失突变体,并通过瞬时表达试验检测了腺嘌呤磷酸核糖转移酶(APRT)或氯霉素乙酰转移酶(CAT)的活性。aprt基因使用单一的转录起始位点簇,并且缺乏真核启动子的一般组成部分如TATA和CCAAT等共有序列。启动子序列的5'缺失突变表明:(i)APRT活性或延伸至-89位(相对于主要转录起始位点)的转录均无降低;(ii)额外缺失29个碱基对(bp)会使APRT活性和转录降低两倍;(iii)转录起始位点之后的缺失(P5'δ+27)会使APRT活性和转录均消失,这表明主要转录起始位点上游紧邻的一个60-bp片段参与基础转录,而该60-bp片段上游紧邻的一个29-bp片段会使转录增强两倍。3'缺失突变表明,5'前导序列和编码序列中一个61-bp片段的缺失会使aprt-CAT基因转录本的有效翻译消失。此外,在基因组3'端有两个聚腺苷酸化信号,近端的那个信号足以进行功能性聚腺苷酸化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0162/363454/b3460d94d941/molcellb00066-0283-a.jpg

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