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细菌糖原合成的relA基因控制

relA Gene control of bacterial glycogen synthesis.

作者信息

Bridger W A, Paranchych W

出版信息

Can J Biochem. 1978 Jun;56(6):403-6. doi: 10.1139/o78-063.

Abstract

Starvation of Escherichia coli K12 for an amino acid results in the stimulation of bacterial glycogen synthesis in cells containing the relA+ gene, but not in cells carrying the relA- allele. Similarly, a large difference in glycogen content is demonstrable between relA+ and relA- cells in stationary phase. It is concluded that guanosine 5',3' -bis(diphosphate) (ppGPP) or some related relA -dependent metabolite is involved in the regulation of bacterial glycogen synthesis. Detection of significant basal levels of glycogen in a relA- strain of E. coli and in unstarved relA+ C. coli indicates that relA control is not absolutely required for glycogen synthesis but serves as a signal for modulation in response to nutrient availability.

摘要

使大肠杆菌K12缺乏一种氨基酸,会导致在含有relA+基因的细胞中刺激细菌糖原合成,但在携带relA-等位基因的细胞中则不会。同样,在稳定期,relA+和relA-细胞之间的糖原含量存在明显差异。得出的结论是,鸟苷5',3'-双(二磷酸)(ppGPP)或一些相关的relA依赖性代谢物参与细菌糖原合成的调节。在大肠杆菌的relA-菌株和未饥饿的relA+大肠杆菌中检测到显著的基础糖原水平,这表明relA调控对于糖原合成并非绝对必需,但可作为响应营养可用性进行调节的信号。

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