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类λ噬菌体的cII样蛋白与pRE样启动子之间的交叉特异性

Cross-specificities between cII-like proteins and pRE-like promoters of lambdoid bacteriophages.

作者信息

Wulff D L, Mahoney M E

出版信息

Genetics. 1987 Apr;115(4):597-604. doi: 10.1093/genetics/115.4.597.

Abstract

We have investigated the activation of transcription from the pRE promoters of phages lambda, 21 and P22 by the lambda and 21 cII proteins and the P22 c1 (cII-like) protein, using an in vivo system in which cII protein from a derepressed prophage activates transcription from a pRE DNA fragment on a multicopy plasmid. We find that each protein is highly specific for its own cognate pRE promoter, although measureable cross-reactions are observed. The primary recognition sequence for cII protein on lambda pRE is a pair of TTGC repeat sequences in the sequence 5'-TTGCN6TTGC-3' at the -35 region of the promoter. This same sequence is found in 21 pRE, while P22 pRE has the sequence 5'-TTGCN6TTGT-3', which is the same as that of lambda ctr1, a pRE+ variant of lambda. lambda ctr1 pRE is half as active as lambda + pRE when assayed with either the lambda cII or the P22 c1 proteins. Therefore, the single base change in the P22 repeat sequence cannot explain why the P22 c1 protein is much more active with P22 pRE than lambda pRE. The dya5 mutation, a G----A change at position -43 of pRE, makes pRE a stronger promoter when assayed with either the lambda or 21 cII proteins or the P22 c1 protein. We conclude that efficient activation of a cII-dependent promoter by a cII protein requires sequence information in addition to the TTGC repeat sequences. We do not know the characteristics of the proteins which are responsible for the specificity of each protein for its own cognate promoter.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们利用一种体内系统,研究了λ噬菌体、21噬菌体和P22噬菌体的pRE启动子被λ和21的cII蛋白以及P22的c1(类cII)蛋白激活的情况。在该系统中,来自去阻遏原噬菌体的cII蛋白激活多拷贝质粒上pRE DNA片段的转录。我们发现,尽管观察到了可测量的交叉反应,但每种蛋白对其自身的同源pRE启动子具有高度特异性。λ噬菌体pRE上cII蛋白的主要识别序列是启动子-35区域中5'-TTGCN6TTGC-3'序列中的一对TTGC重复序列。21噬菌体的pRE中也发现了相同的序列,而P22噬菌体的pRE具有5'-TTGCN6TTGT-3'序列,这与λ噬菌体的pRE +变体λctr1的序列相同。用λ cII蛋白或P22 c1蛋白检测时,λctr1 pRE的活性是λ + pRE的一半。因此,P22重复序列中的单个碱基变化无法解释为什么P22 c1蛋白对P22 pRE的活性比对λ pRE的活性高得多。dya5突变是pRE - 43位的G→A变化,在用λ或21的cII蛋白或P22 c1蛋白检测时,使pRE成为更强的启动子。我们得出结论,cII蛋白对cII依赖性启动子的有效激活除了需要TTGC重复序列外,还需要序列信息。我们不知道负责每种蛋白对其自身同源启动子特异性的蛋白质的特征。(摘要截短于250字)

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