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乙醛酸旁路操纵子阻遏物编码基因iclR的自动调节。

Autoregulation of iclR, the gene encoding the repressor of the glyoxylate bypass operon.

作者信息

Gui L, Sunnarborg A, Pan B, LaPorte D C

机构信息

Department of Biochemistry, University of Minnesota, Minneapolis 55455, USA.

出版信息

J Bacteriol. 1996 Jan;178(1):321-4. doi: 10.1128/jb.178.1.321-324.1996.

DOI:10.1128/jb.178.1.321-324.1996
PMID:8550439
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC177660/
Abstract

The aceBAK operon was partially induced by a multicopy plasmid which carried the promoter region of the gene which encodes its repressor, iclR. Gel shift and DNase I analyses demonstrated that IclR binds to its own promoter. Disruption of iclR increased the expression of an iclR::lacZ operon fusion. Although aceBAK and iclR are both regulated by IclR, aceBAK expression responds to the carbon source, while expression of iclR does not.

摘要

aceBAK操纵子被携带编码其阻遏物iclR基因启动子区域的多拷贝质粒部分诱导。凝胶迁移和DNA酶I分析表明,IclR与其自身的启动子结合。iclR的破坏增加了iclR::lacZ操纵子融合体的表达。尽管aceBAK和iclR都受IclR调控,但aceBAK的表达对碳源有反应,而iclR的表达则无此反应。

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