Metal-dependent gene regulation in the causative agent of lyme disease

Bryan Troxell, X. Yang

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Borrelia burgdorferi (Bb) is the causative agent of Lyme disease transmitted to humans by ticks of the Ixodes spp. Bb is a unique bacterial pathogen because it does not require iron (Fe2+) for its metabolism. Bb encodes a ferritin-like Dps homolog called NapA (also called BicA), which can bind Fe or copper (Cu2+), and a manganese (Mn2+) transport protein, Borrelia metal transporter A (BmtA); both proteins are required for colonization of the tick vector, but BmtA is also required for the murine host. This demonstrates that Bb's metal homeostasis is a critical facet of the complex enzootic life cycle between the arthropod and murine hosts. Although metals are known to influence the expression of virulence determinants during infection, it is unknown how or if metals regulate virulence in Bb. Recent evidence demonstrates that Bb modulates the intracellular Mn2+ and zinc (Zn2+) content and, in turn, these metals regulate gene expression through influencing the Ferric Uptake Regulator (Fur) homolog Borrelia Oxidative Stress Regulator (BosR). This mini-review focuses on the burgeoning study of metal-dependent gene regulation within Bb.

Original languageEnglish
Article number79
JournalFrontiers in cellular and infection microbiology
Volume4
Issue numberNOV
DOIs
StatePublished - 2013

Fingerprint

Lyme Disease
Borrelia burgdorferi
Metals
Borrelia
Genes
Ticks
Virulence
Ixodes
Arthropods
Ferritins
Manganese
Life Cycle Stages
Zinc
Copper
Carrier Proteins
Oxidative Stress
Homeostasis
Iron
Gene Expression
Infection

Keywords

  • Borrelia burgdorferi
  • Calprotectin
  • Copper
  • Lyme disease
  • Manganese
  • Zinc

ASJC Scopus subject areas

  • Microbiology
  • Microbiology (medical)
  • Infectious Diseases
  • Immunology
  • Medicine(all)

Cite this

Metal-dependent gene regulation in the causative agent of lyme disease. / Troxell, Bryan; Yang, X.

In: Frontiers in cellular and infection microbiology, Vol. 4, No. NOV, 79, 2013.

Research output: Contribution to journalArticle

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