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不动杆菌属ADP1菌株转录调节因子PcaU所发挥的作用。

Effects exerted by transcriptional regulator PcaU from Acinetobacter sp. strain ADP1.

作者信息

Trautwein G, Gerischer U

机构信息

Department of Microbiology and Biotechnology, University of Ulm, 89069 Ulm, Germany.

出版信息

J Bacteriol. 2001 Feb;183(3):873-81. doi: 10.1128/JB.183.3.873-881.2001.

Abstract

Protocatechuate degradation is accomplished in a multistep inducible catabolic pathway in Acinetobacter sp. strain ADP1. The induction is brought about by the transcriptional regulator PcaU in concert with the inducer protocatechuate. PcaU, a member of the new IclR family of transcriptional regulators, was shown to play a role in the activation of transcription at the promoter for the structural pca genes, leaving open the participation of additional activators. In this work we show that there is no PcaU-independent transcriptional activation at the pca gene promoter. The minimal inducer concentration leading to an induction response is 10(-5) M protocatechuate. The extent of expression of the pca genes was observed to depend on the nature of the inducing carbon source, and this is assumed to be caused by different internal levels of protocatechuate in the cells. The basal level of expression was shown to be comparatively high and to vary depending on the noninducing carbon source independent of PcaU. In addition to the activating function, in vivo results suggest a repressing function for PcaU at the pca gene promoter in the absence of an elevated inducer concentration. Expression at the pcaU gene promoter is independent of the growth condition but is subject to strong negative autoregulation. We propose a model in which PcaU exerts a repressor function both at its own promoter and at the structural gene promoter and in addition functions as an activator of transcription at the structural gene promoter at elevated inducer concentration.

摘要

原儿茶酸的降解是在不动杆菌属ADP1菌株的多步诱导分解代谢途径中完成的。这种诱导是由转录调节因子PcaU与诱导剂原儿茶酸协同作用实现的。PcaU是转录调节因子新IclR家族的成员,已证明它在结构pca基因启动子处的转录激活中发挥作用,但其他激活剂的参与情况尚不清楚。在这项研究中,我们表明在pca基因启动子处不存在不依赖PcaU的转录激活。导致诱导反应的最低诱导剂浓度是10^(-5) M原儿茶酸。观察到pca基因的表达程度取决于诱导碳源的性质,这被认为是由细胞中原儿茶酸的不同内部水平引起的。已表明基础表达水平相对较高,并且取决于不依赖PcaU的非诱导碳源。除了激活功能外,体内结果表明在诱导剂浓度未升高时,PcaU在pca基因启动子处具有抑制功能。pcaU基因启动子处的表达与生长条件无关,但受到强烈的负自调节。我们提出了一个模型,其中PcaU在其自身启动子和结构基因启动子处均发挥阻遏功能,此外在诱导剂浓度升高时作为结构基因启动子处的转录激活剂发挥作用。

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