Absence of Global Stress Regulation in Escherichia coli Promotes Pathoadaptation and Novel c-di-GMP-dependent

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Nikola Zlatkov1, Bernt Eric Uhlin2

  • 1The Laboratory for Molecular Infection Medicine Sweden (MIMS), Department of Molecular Biology, Umeå University, Umea, Sweden.

Scientific Reports
|February 24, 2019
PubMed

Insights

Neonatal meningitis-causing E. coli (NMEC) utilizes unique metabolic pathways, including aerobic citrate use, by inactivating the RpoS regulator. This adaptation, linked to cyclic di-GMP (c-di-GMP) signaling, aids NMEC survival and pathogenesis.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Molecular Biology

Background:

  • Neonatal meningitis-causing Escherichia coli (NMEC) harbors pathoadaptive mutations affecting cyclic di-GMP (c-di-GMP) signaling.
  • RpoS, a global stress regulator, influences c-di-GMP levels, impacting bacterial sessility and motility.

Purpose of the Study:

  • To investigate the role of pathoadaptive mutations in c-di-GMP signaling in NMEC.
  • To understand the metabolic adaptations of NMEC, particularly aerobic citrate utilization.
  • To elucidate the connection between RpoS, c-di-GMP, and NMEC virulence factors like S-fimbriae.

Main Methods:

  • Analysis of NMEC strains with varying RpoS and ycgG2 gene status.
  • Assessment of c-di-GMP levels and S-fimbriae production.
  • Investigation of aerobic citrate utilization in the presence of glucose.
  • Reconstitution of metabolic abilities in E. coli UTI89 and analysis of pyelonephritis isolates.

Main Results:

  • NMEC strains deficient in RpoS showed low c-di-GMP levels.
  • Deletion of ycgG2 and RpoS restoration decreased S-fimbriae production, suggesting the urinary tract as a potential NMEC habitat.
  • NMEC exhibited aerobic citrate utilization with glucose, a novel trait for E. coli, linked to RpoS inactivation.
  • RpoS inactivation leads to CitT transporter production for ferric citrate uptake, dependent on YcgG2's phosphodiesterase activity.

Conclusions:

  • RpoS inactivation is key to NMEC's unique aerobic citrate utilization, enabling ferric citrate uptake via CitT.
  • YcgG2, a c-di-GMP phosphodiesterase allozyme, plays a crucial role in this metabolic adaptation.
  • These findings highlight NMEC's specialized pathoadaptive strategies for survival and pathogenesis, potentially involving the urinary tract.

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