首页> 美国卫生研究院文献>Journal of Bacteriology >Role of the Escherichia coli FadR regulator in stasis survival and growth phase-dependent expression of the uspA fad and fab genes.
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Role of the Escherichia coli FadR regulator in stasis survival and growth phase-dependent expression of the uspA fad and fab genes.

机译:大肠杆菌FadR调节剂在uspAfad和fab基因的停滞存活和生长阶段依赖性表达中的作用。

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摘要

The increased expression of the uspA gene of Escherichia coli is an essential part of the cell's response to growth arrest. We demonstrate that stationary-phase activation of the uspA promoter is in part dependent on growth phase-dependent inactivation or repression of the FadR regulator. Transcription of uspA is derepressed during exponential growth in fadR null mutants or by including the fatty acid oleate in the growth medium of FadR+ cells. The results of DNA footprinting analysis show that FadR binds downstream of the uspA promoter in the noncoding region. Thus, uspA is a member of the fadR regulon. All the fad-lacZ fusions examined (fadBA, fadL, and fadD) are increasingly expressed in stationary phase with kinetics similar to that of the increased expression of uspA. In contrast, beta-galactosidase levels decrease during stationary phase in a fabA-lacZ lysogen, consistent with the role of FadR as an activator of fabA. The growth phase-dependent increased and decreased transcription of fad genes and fabA, respectively, is dependent on the status of the fadR gene. Cells carrying a mutation in the FadR gene (fadRS219N) that makes it nonderepressible exhibit a weak stationary-phase induction of uspA and fad genes. In addition, cells carrying fadRS219N survive long-term stasis poorly, indicating that FadR-dependent alterations in fatty acid metabolism are an integral and important part of the adaptation to stationary phase.
机译:大肠杆菌uspA基因表达的增加是细胞对生长停滞反应的重要组成部分。我们证明,uspA启动子的固定相激活部分取决于FadR调节剂的生长相依赖性失活或抑制。在fadR null突变体的指数生长过程中或通过在FadR +细胞的生长培养基中加入脂肪酸油酸酯,uspA的转录被抑制。 DNA足迹分析的结果表明,FadR在非编码区与uspA启动子的下游结合。因此,uspA是fadR法规的成员。所有检测到的fad-lacZ融合体(fadBA,fadL和fadD)在固定相中的表达逐渐增加,其动力学类似于uspA表达增加的动力学。相反,在fabA-lacZ溶原菌中,β-半乳糖苷酶水平在固定阶段降低,这与FadR作为fabA激活剂的作用一致。 fad基因和fabA分别依赖于生长阶段的转录增加和减少取决于fadR基因的状态。 FadR基因突变(fadRS219N)使其无法抑制的细胞表现出弱的uspA和fad基因固定相诱导。此外,携带fadRS219N的细胞无法长期生存,表明脂肪酸代谢中FadR依赖性改变是适应固定期不可或缺的重要组成部分。

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