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Related Experiment Video

Updated: Jan 31, 2026

Development of a Larval Zebrafish Infection Model for Clostridioides difficile
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Iron Regulation in Clostridioides difficile.

Mareike Berges1, Annika-Marisa Michel1, Christian Lassek2

  • 1Braunschweig Integrated Centre of Systems Biology (BRICS), Technische Universität Braunschweig, Braunschweig, Germany.

Frontiers in Microbiology
|January 9, 2019
PubMed
Summary
This summary is machine-generated.

The ferric uptake regulator (Fur) controls how Clostridioides difficile adapts to low iron, impacting metabolism, cell surface, and motility. This study reveals Fur

Keywords:
Furcell walliron regulationiron transportmetabolismpolyamine

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • The ferric uptake regulator (Fur) is a key transcriptional regulator controlling iron homeostasis in bacteria.
  • Clostridioides difficile, an opportunistic Gram-positive pathogen, relies on intricate regulatory networks for survival and virulence.
  • Understanding Fur-mediated regulation in C. difficile is crucial for deciphering its adaptive strategies under nutrient-limited conditions.

Purpose of the Study:

  • To comprehensively investigate the Fur-regulated transcriptional, translational, and metabolic networks in Clostridioides difficile.
  • To elucidate the adaptive responses of C. difficile to iron limitation.
  • To identify direct and indirect targets of Fur in C. difficile.

Main Methods:

  • Combined transcriptomic (RNA sequencing), proteomic, and metabolomic analyses.
  • Electron microscopy for cell wall and flagella visualization.
  • Construction and characterization of a C. difficile fur mutant.

Main Results:

  • Fur regulates iron and siderophore transporters, central energy metabolism, and amino acid fermentation pathways.
  • Low iron conditions induce flavodoxin and riboflavin biosynthesis, while downregulating ferredoxin-dependent pathways.
  • The fur mutant exhibits altered ATP synthesis, increased sensitivity to antibiotics, cell wall remodeling, loss of flagella, and reduced motility.

Conclusions:

  • Adaptation to low iron in C. difficile involves enhanced iron import and metabolic pathway replacement, with Fur playing a central role.
  • Fur directly regulates a subset of genes, while broader metabolic and cellular adaptations occur indirectly.
  • The findings provide insights into C. difficile's survival mechanisms and potential therapeutic targets.