Metabolic block at early stages of the glycolytic pathway activates the Rcs phosphorelay system via increased synthesis of dTDP-glucose in Escherichia coli

Waleed El-Kazzaz, Teppel Morita, Hideaki Tagami, Toshifumi Inada, Hiroji Aiba

研究成果: Article査読

25 被引用数 (Scopus)

抄録

A mutational block in the early stages of the glycolytic pathway facilitates the degradation of the ptsG mRNA encoding the major glucose transporter IICBGlc in Escherichia coli. The degradation is RNase E dependent and is correlated with the accumulation of either glucose-6-P or fructose-6-P (Kimata et al., 2001, EMBO J 20: 3587-3595; Morita et al., 2003, J Biol Chem 278: 15608-15614). In this paper, we investigate additional physiological effects resulting from the accumulation of glucose-6-P caused by a mutation in pgi encoding phosphoglucose isomerase, focusing on changes in gene expression. The addition of glucose to the pgi strain caused significant growth inhibition, in particular in the mlc background. Cell growth then gradually resumed as the level of IICBGlc decreased. We found that the transcription of the cps operon, encoding a series of proteins responsible for the synthesis of colanic acid, was markedly but transiently induced under this metabolic stress. Both genetic and biochemical studies revealed that the metabolic stress Induces cps transcription by activating the RcsC/YojN/RcsB signal transductlon system. Overexpression of glucose-6-P dehydrogenase eliminated both growth inhibition and cps induction by reducing the glucose-6-P level. Mutations in genes responsible for the synthesis of glucose-1-P and/or dTDP-glucose eliminated the activation of the Res system by the metabolic stress. Taken together, we conclude that an increased synthesis of dTDP-glucose activates the Rcs phosphorelay system, presumably by affecting the synthesis of oligosaccharides for enterobacterial common antigen and O-antigen.

本文言語English
ページ(範囲)1117-1128
ページ数12
ジャーナルMolecular Microbiology
51
4
DOI
出版ステータスPublished - 2004 2月
外部発表はい

ASJC Scopus subject areas

  • 微生物学
  • 分子生物学

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