Suppr超能文献

核糖核酸酶III对信使核糖核酸的加工调控噬菌体T7基因1.2的表达。

Processing of mRNA by ribonuclease III regulates expression of gene 1.2 of bacteriophage T7.

作者信息

Saito H, Richardson C C

机构信息

Department of Biological Chemistry, Harvard Medical School, Boston, Massachusetts 02115.

出版信息

Cell. 1981 Dec;27(3 Pt 2):533-42. doi: 10.1016/0092-8674(81)90395-0.

Abstract

A bacteriophage T7 mutation, HS9, is phenotypically defective in gene 1.2, although it maps outside the gene. The single nucleotide change responsible for the HS9 mutation lies within the RNAase III recognition site immediately following gene 1.2. This RNAase III recognition site, responsible for the processing of the mRNA encoding genes 1.1 and 1.2, contains two cleavage sites, separated by 29 bases. The HS9 mutation prevents cutting by RNAase III at one site in vitro, yielding a mRNA containing an additional 29 bases at its 3' end. The ten second-site reversion mutations of HS9 are all located in the RNAase III recognition site and either restore or eliminate cutting at both sites. RNAase III mutants of Escherichia coli phenotypically suppress the HS9 mutation. We propose that the extra 29 bases at the 3' end of the mRNA hybridize to the ribosome-binding site of gene 1.1; gene 1.1 immediately precedes gene 1.2 on the same mRNA molecule. Such hybridization prevents the initiation of translation of this mRNA containing gene 1.1. A strong polar effect represses the translation of gene 1.2.

摘要

噬菌体T7突变体HS9在基因1.2上表现出表型缺陷,尽管其定位在该基因之外。导致HS9突变的单核苷酸变化位于紧跟基因1.2之后的RNA酶III识别位点内。这个负责加工编码基因1.1和1.2的mRNA的RNA酶III识别位点包含两个切割位点,相隔29个碱基。HS9突变在体外阻止RNA酶III在一个位点的切割,产生一个在其3'端含有额外29个碱基的mRNA。HS9的十个第二位点回复突变都位于RNA酶III识别位点,并且恢复或消除了两个位点的切割。大肠杆菌的RNA酶III突变体表型上抑制了HS9突变。我们提出,mRNA 3'端额外的29个碱基与基因1.1的核糖体结合位点杂交;基因1.1在同一mRNA分子上紧接在基因1.2之前。这种杂交阻止了包含基因1.1的该mRNA的翻译起始。一种强烈的极性效应抑制了基因1.2的翻译。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验