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鼠伤寒沙门氏菌中钴胺酰胺生物合成基因的氧化还原调节

Redox regulation of the genes for cobinamide biosynthesis in Salmonella typhimurium.

作者信息

Andersson D I, Roth J R

机构信息

Department of Biology, University of Utah, Salt Lake City 84112.

出版信息

J Bacteriol. 1989 Dec;171(12):6734-9. doi: 10.1128/jb.171.12.6734-6739.1989.

Abstract

Transcription of the cobinamide biosynthetic genes (the CobI operon) was induced under three different physiological conditions: anaerobiosis (anaerobic respiration or fermentation), aerobic respiration at low oxygen levels, and aerobic respiration with a partial block of the electron transport chain. After a shift to inducing conditions, there was a time lag of approximately 50 min before the onset of CobI induction. Under conditions of anaerobic respiration, the level of CobI transcription was dependent on the nature of both the electron donor (carbon and energy source) and the acceptor. Cells grown with electron acceptors with a lower midpoint potential showed higher CobI expression levels. The highest level of CobI transcription observed was obtained with glycerol as the carbon source and fumarate as the electron acceptor. The high induction seen with glycerol was reduced by mutational blocks in the glycerol catabolic pathway, suggesting that glycerol does not serve as a gratuitous inducer but must be metabolized to stimulate CobI transcription. In the presence of oxygen, CobI operon expression was induced 6- to 20-fold by the following: inhibition of cytochrome o oxidase with cyanide, mutational blockage of ubiquinone biosynthesis, and starvation of mutant cells for heme. We suggest that the CobI operon is induced in response to a reducing environment within the cell and not by the absence of oxygen per se.

摘要

钴胺酰胺生物合成基因(CobI操纵子)的转录在三种不同的生理条件下被诱导:无氧状态(无氧呼吸或发酵)、低氧水平下的有氧呼吸以及电子传递链部分受阻的有氧呼吸。转变为诱导条件后,CobI诱导开始前有大约50分钟的时间延迟。在无氧呼吸条件下,CobI转录水平取决于电子供体(碳源和能源)和受体的性质。用中点电位较低的电子受体培养的细胞显示出较高的CobI表达水平。观察到的最高CobI转录水平是以甘油作为碳源和富马酸作为电子受体时获得的。甘油分解代谢途径中的突变阻断降低了甘油所导致的高诱导作用,这表明甘油并非作为一种 gratuitous诱导剂,而是必须被代谢才能刺激CobI转录。在有氧存在的情况下,通过以下方式可使CobI操纵子表达诱导6至20倍:用氰化物抑制细胞色素o氧化酶、泛醌生物合成的突变阻断以及突变细胞的血红素饥饿。我们认为,CobI操纵子是响应细胞内的还原环境而被诱导,而非仅仅因为缺氧本身。

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