大肠杆菌中泛醌含量低会导致硫醇超敏反应。
Low ubiquinone content in Escherichia coli causes thiol hypersensitivity.
作者信息
Zeng H, Snavely I, Zamorano P, Javor G T
机构信息
Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, California 92350, USA.
出版信息
J Bacteriol. 1998 Jul;180(14):3681-5. doi: 10.1128/JB.180.14.3681-3685.1998.
Abstract
Thiol hypersensitivity in a mutant of Escherichia coli (IS16) was reversed by complementation with a plasmid that carried the ubiX gene. The mutant had low ubiquinone content. Complementation elevated the ubiquinone level and eliminated thiol hypersensitivity. Analysis of chromosomal ubiX genes indicated that both parent and mutant strains were ubiX mutants. The low ubiquinone content of IS16 was possibly caused by a ubiD ubiX genotype. A ubiA mutant also exhibited thiol hypersensitivity. Neither IS16 nor the ubiA mutant strain could produce alkaline phosphatase (in contrast to their parent strains) after 2 h of induction, thus showing Dsb- phenotypes. The phenomena of thiol hypersensitivity and low ubiquinone content may be linked by their connections to the periplasmic disulfide bond redox machinery.
摘要
通过用携带ubiX基因的质粒进行互补，可逆转大肠杆菌突变体（IS16）中的硫醇超敏反应。该突变体的泛醌含量较低。互补作用提高了泛醌水平并消除了硫醇超敏反应。对染色体ubiX基因的分析表明，亲本菌株和突变菌株都是ubiX突变体。IS16泛醌含量低可能是由ubiD ubiX基因型引起的。ubiA突变体也表现出硫醇超敏反应。诱导2小时后，IS16和ubiA突变体菌株均不能产生碱性磷酸酶（与其亲本菌株相反），因此表现出Dsb-表型。硫醇超敏反应和泛醌含量低的现象可能通过它们与周质二硫键氧化还原机制的联系而相互关联。
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