English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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 (Fe 2+ ) for its metabolism.  Bb  encodes a ferritin-like Dps homolog called NapA (also called BicA), which can bind Fe or copper (Cu 2+ ), and a manganese (Mn 2+ ) 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 Mn 2+  and zinc (Zn 2+ ) 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 .

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