Interaction of Borrelia burgdorferi Hbb with the p66 promoter

Melisa S Medrano1, Paul F Policastro, Tom G Schwan

  • 1Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA 02111, USA.

Nucleic Acids Research
|November 14, 2009
PubMed

Insights

Researchers identified Hbb as a key regulator of P66 expression in Borrelia burgdorferi, the bacterium causing Lyme disease. Hbb influences P66 levels during tick transmission, impacting Lyme disease pathogenesis.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Infectious Diseases

Background:

  • Borrelia burgdorferi causes Lyme disease and expresses the P66 protein, an integrin ligand.
  • P66 expression varies depending on the bacterium's environment, including during tick transmission.

Purpose of the Study:

  • To identify bacterial factors regulating P66 expression in Borrelia burgdorferi.
  • To elucidate the role of candidate transcription factors in P66 gene regulation.

Main Methods:

  • Utilized a reporter gene assay in E. coli with a p66 promoter-alkaline phosphatase fusion.
  • Screened Borrelia burgdorferi genome for transcription factor homologs.
  • Investigated binding of candidate transcription factors to the p66 promoter.

Main Results:

  • Identified three candidate transcription factors: BBA23 (increased activity), Hbb (BB0232), and BB0527 (decreased activity).
  • Hbb (BB0232) demonstrated binding to the p66 promoter, unlike BBA23 and BB0527.
  • Expression patterns of p66 and Hbb in ticks suggest Hbb regulates p66.

Conclusions:

  • Hbb (BB0232) is implicated as a regulator of P66 expression in Borrelia burgdorferi.
  • Understanding P66 regulation by Hbb may offer insights into Lyme disease transmission and pathogenesis.