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大肠杆菌中uidR基因的负显性突变:uidA基因表达协同调控的遗传学证据

Negative dominant mutations of the uidR gene in Escherichia coli: genetic proof for a cooperative regulation of uidA expression.

作者信息

Blanco C, Ritzenthaler P, Mata-Gilsinger M

出版信息

Genetics. 1986 Feb;112(2):173-82. doi: 10.1093/genetics/112.2.173.

Abstract

The uidA gene is the first gene involved in the hexuronide-hexuronate pathway in Escherichia coli K-12 and is under the dual control of the uidR and uxuR encoded repressors. Point mutations affecting the uidR regulatory gene were sought to investigate the regulation of uidA. When the uidR mutant allele was on a multicopy plasmid and the wild-type allele was on the chromosome, some of the mutant phenotypes were dominant to the wild-type phenotype, indicating that the active form of the UidR repressor is multimeric. We have demonstrated that expression of the mutant phenotype is dependent on gene dosage. The dominance of the uidR allele was also sensitive to the presence of the wild-type uxuR allele in the cell. This behavior probably results from UidR-UxuR repressor interactions. A mechanism is proposed: we suggest that the UidR and UxuR repressors interact after their binding to the operator site of uidA; the binding of one regulatory molecule may facilitate the binding of the other one in a cooperative process.

摘要

uidA基因是大肠杆菌K-12中参与己糖醛酸-己糖醛酸盐途径的首个基因,受uidR和uxuR编码的阻遏物双重调控。为了研究uidA的调控机制,我们寻找了影响uidR调控基因的点突变。当uidR突变等位基因位于多拷贝质粒上,而野生型等位基因位于染色体上时,一些突变表型对野生型表型呈显性,这表明UidR阻遏物的活性形式是多聚体。我们已经证明突变表型的表达取决于基因剂量。uidR等位基因的显性也对细胞中野生型uxuR等位基因的存在敏感。这种行为可能是由于UidR-UxuR阻遏物相互作用所致。我们提出了一种机制:我们认为UidR和UxuR阻遏物在它们结合到uidA的操纵位点后相互作用;在协同过程中,一种调节分子的结合可能促进另一种调节分子的结合。

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