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Quantifying Yersinia pseudotuberculosis Type III Secretion System Activity Following Iron Starvation and Anaerobic Growth
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Tailoring a Global Iron Regulon to a Uropathogen.

Rajdeep Banerjee1, Erin Weisenhorn1, Kevin J Schwartz2

  • 1Department of Biomolecular Chemistry, University of Wisconsin-Madison, Madison, Wisconsin, USA.

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Summary

The ferric uptake regulator (Fur) controls iron homeostasis in uropathogenic Escherichia coli (UPEC). UPEC

Keywords:
CFT073FurRyhBSigma SUPECiron regulationmetabolic adaptationppGpp

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Bacterial Pathogenesis

Background:

  • Pathogenicity islands and plasmids contribute to Escherichia coli virulence.
  • Regulatory networks' role in disease phenotypes is less understood.
  • Iron homeostasis is crucial for bacterial survival and pathogenesis.

Purpose of the Study:

  • To dissect the regulatory network governed by the ferric uptake regulator (Fur) in uropathogenic E. coli (UPEC).
  • To compare Fur regulons between UPEC and commensal E. coli K-12.
  • To understand how Fur-mediated regulation impacts bacterial adaptation to host environments.

Main Methods:

  • Genome-scale DNA binding assays for Fur.
  • Transcriptomic and proteomic analyses of UPEC and E. coli K-12.
  • Analysis of gene expression and protein levels under varying conditions (anaerobic, aerobic, iron chelation).

Main Results:

  • The Fur regulon in UPEC is conserved but also includes genes on pathogenicity islands.
  • UPEC fur mutants showed unexpected activation of amino acid limitation and general stress responses.
  • Amino acid addition mitigated stress in UPEC fur mutants; iron chelation mimicked this effect.
  • Aerobic conditions exacerbated amino acid demand, linked to aerobactin synthesis.

Conclusions:

  • Fur regulation in UPEC links iron homeostasis to amino acid demand and stress responses.
  • This coordinated response may be critical for UPEC survival in nutrient-limited urinary tract environments.
  • The coupling of iron limitation response to increased amino acid demand differentiates UPEC from other E. coli pathotypes.