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CreA阻遏蛋白是唯一一种通过与几个特定位点结合来负责构巢曲霉中alcA基因碳分解代谢阻遏的DNA结合蛋白。

The CreA repressor is the sole DNA-binding protein responsible for carbon catabolite repression of the alcA gene in Aspergillus nidulans via its binding to a couple of specific sites.

作者信息

Panozzo C, Cornillot E, Felenbok B

机构信息

Institut de Génétique et Microbiologie, Université Paris-Sud, URA CNRS D 2225, Centre Universitaire d'Orsay, Bâtiment 409, F-91405 Orsay Cedex, France.

出版信息

J Biol Chem. 1998 Mar 13;273(11):6367-72. doi: 10.1074/jbc.273.11.6367.

Abstract

Carbon catabolite repression is mediated in Aspergillus nidulans by the negative acting protein CreA. The CreA repressor plays a major role in the control of the expression of the alc regulon, encoding proteins required for the ethanol utilization pathway. It represses directly, at the transcriptional level, the specific transacting gene alcR, the two structural genes alcA and aldA, and other alc genes in all physiological growth conditions. Among the seven putative CreA sites identified in the alcA promoter region, we have determined the CreA functional targets in AlcR constitutive and derepressed genetic backgrounds. Two different divergent CreA sites, of which one overlaps a functional AlcR inverted repeat site, are largely responsible for alcA repression. Totally derepressed alcA expression is achieved when these two CreA sites are disrupted in addition to another single site, which overlaps the functional palindromic induction target. The fact that derepression is always associated with alcA overexpression is consistent with a competition model between AlcR and CreA for their cognate targets in the same region of the alcA promoter. Our results also indicate that the CreA repressor is necessary and sufficient for the total repression of the alcA gene.

摘要

在构巢曲霉中,碳分解代谢物阻遏由负调控蛋白CreA介导。CreA阻遏物在乙醇利用途径所需蛋白质编码的alc操纵子表达调控中起主要作用。在所有生理生长条件下,它在转录水平直接抑制特异性反式作用基因alcR、两个结构基因alcA和aldA以及其他alc基因。在alcA启动子区域鉴定出的七个假定CreA位点中,我们已经确定了在AlcR组成型和去阻遏遗传背景下的CreA功能靶点。两个不同的反向CreA位点,其中一个与功能性AlcR反向重复位点重叠,在很大程度上负责alcA的阻遏。当这两个CreA位点与另一个与功能性回文诱导靶点重叠的单个位点一起被破坏时,可实现完全去阻遏的alcA表达。去阻遏总是与alcA过表达相关这一事实与AlcR和CreA在alcA启动子同一区域的同源靶点竞争模型一致。我们的结果还表明,CreA阻遏物对于alcA基因的完全阻遏是必要且充分的。

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