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截短的AraC蛋白对ara操纵子的激活不需要诱导剂。

Activation of ara operons by a truncated AraC protein does not require inducer.

作者信息

Menon K P, Lee N L

机构信息

Department of Biological Sciences, University of California, Santa Barbara 93106.

出版信息

Proc Natl Acad Sci U S A. 1990 May;87(10):3708-12. doi: 10.1073/pnas.87.10.3708.

Abstract

The araC gene of Escherichia coli encodes a protein that binds the inducer L-arabinose to activate the transcription of three ara operons. In a study to determine the functional domains within the AraC protein, we have generated a set of overlapping deletions from the proximal end of the araC gene. We found that the removal of up to nearly 60% of the coding sequence of this protein still allows transcriptional activation of the ara operons in vivo, up to 27% that of the wild type. These truncated proteins, however, no longer require arabinose for induction. The ligand-induced conformational change apparently either releases or unmasks an existing functional domain within AraC, rather than generating a new conformation that is required for activation of the promoter of araBAD. Since the truncated protein of the mutant C154 (which lacks 153 amino acid residues from the N terminus) retains DNA binding specificity, the DNA-recognition domain is localized in the C-terminal half of the AraC protein. Truncated proteins were unable to repress araBAD or araC in vivo, even though they were able to bind all ara operators. We propose that the N-terminal half of AraC is essential for the formation of the DNA loops that are responsible for repression of araBAD and for autoregulation of araC.

摘要

大肠杆菌的araC基因编码一种蛋白质,该蛋白质可结合诱导剂L-阿拉伯糖以激活三个ara操纵子的转录。在一项确定AraC蛋白功能结构域的研究中,我们从araC基因的近端产生了一组重叠缺失。我们发现,去除该蛋白高达近60%的编码序列仍能在体内激活ara操纵子的转录,可达野生型的27%。然而,这些截短的蛋白质不再需要阿拉伯糖来诱导。配体诱导的构象变化显然要么释放要么暴露了AraC内现有的功能结构域,而不是产生激活araBAD启动子所需的新构象。由于突变体C154的截短蛋白(从N端缺少153个氨基酸残基)保留了DNA结合特异性,DNA识别结构域位于AraC蛋白的C端一半。截短的蛋白质在体内无法抑制araBAD或araC,即使它们能够结合所有ara操纵基因。我们提出,AraC的N端一半对于形成负责抑制araBAD和araC自调控的DNA环至关重要。

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