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大肠杆菌K-12中半乳糖操纵子在半乳糖操纵基因-启动子区域的调控

Regulation of galactose operon at the gal operator-promoter region in Escherichia coli K-12.

作者信息

Hua S S, Markovitz A

出版信息

J Bacteriol. 1975 May;122(2):510-7. doi: 10.1128/jb.122.2.510-517.1975.

Abstract

The capR (lon) product controls expression of the gal operon independently of the galR repressor. Previously, mutations of the gal operon have been isolated that are semiconstitutive and alter response to the capR and/or capT product. Such mutants imply the existence of a distinct site in the operon that responds to capR (capT) control. This mutation could be either in a site near the operator-distal end of the galE gene, which signals rho factor termination of transcription in vitro or in a site in the operator-promoter region. Bacteriophage U3 was used to isolate galE mutations in HC2142 (a mutant exhibiting reduced response to capR control). P1 transduction was used to cross these mutants with a set of galE gene deletion. Analysis of the resulting Gal+ recombinants indicates that the regulatory site is in the operator-promoter region. Hence, it is unlikely that capR functions in control as an anti-rho factor at the operator-distal end of the galE gene, but more likely as previously suggested, at a second operator distinct from one responding to galR repressor control. Upon induction with D-fucose, a promoter mutant (UV211) isolated previously expressed 20 to 30% of the galactose enzymes that the wild type exhibited in the presence of the inducer D-fucose. The effects of various mutations in cya, capR, and galR on galactokinase synthesis in this mutant were determined. Galactokinase was derepressed by capR as well as galR, but the presence or absence of the cya gene product was unimportant.

摘要

capR(lon)产物独立于galR阻遏物控制gal操纵子的表达。此前,已分离出gal操纵子的突变体,这些突变体是半组成型的,并且改变了对capR和/或capT产物的反应。此类突变体表明操纵子中存在一个对capR(capT)控制有反应的独特位点。该突变可能位于galE基因操纵子远端附近的一个位点,该位点在体外发出rho因子转录终止信号,或者位于操纵子-启动子区域的一个位点。噬菌体U3用于在HC2142(一个对capR控制反应降低的突变体)中分离galE突变。P1转导用于将这些突变体与一组galE基因缺失体进行杂交。对所得Gal+重组体的分析表明,调控位点位于操纵子-启动子区域。因此,capR不太可能在galE基因操纵子远端作为抗rho因子发挥控制作用,而更有可能如先前所提出的,在一个与对galR阻遏物控制有反应的操纵子不同的第二个操纵子处发挥作用。用D-岩藻糖诱导后,先前分离的一个启动子突变体(UV211)表达的半乳糖酶是野生型在诱导剂D-岩藻糖存在下所表现出的20%至30%。确定了cya、capR和galR中的各种突变对该突变体中半乳糖激酶合成的影响。半乳糖激酶可被capR以及galR去阻遏,但cya基因产物的存在与否并不重要。

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