Role of magnesium in the pathophysiology of the agent of Lyme disease

Date

2016

Authors

Smith, Trever C., II

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Abstract

The adaptation of a bacterial pathogen to its host is the summation of the organisms increasing fitness to a specific niche. In some cases, bacteria become pathogenic due to unintended circumstances where an otherwise saprophytic or a non-pathogenic organism causes disease. True bacterial pathogens however, are parasitic in nature and depend on a host. One such bacterial pathogen, Borrelia burgdorferi, persists in nature by cycling between tick vectors and vertebrate hosts. B. burgdorferi, causes Lyme disease, the most prevalent arthropod-borne illness in the US. The borrelial genome is remarkable in that its codes for very few complete biochemical pathways and as a result the bacterium must scavenge biomolecules from its host. Since magnesium is a critical metal for living organisms, I sought out to characterize the role of magnesium (Mg2+) as a virulence signal in B. burgdorferi. Our results indicate that the putative magnesium transporter, MgtE, plays a role in host adaptation by modulating the levels of a major Outer surface protein, OspB. Furthermore, I identified a novel protein, designated as Borrelia host adaptation Protein (BadP), as being essential for the colonization of the mammalian host. In addition, I have investigated potential candidate regulatory RNA species along with the suite of putative RNases that functionally interact to constitute the RNA degradasome in B. burgdorferi. Taken together, these studies have increased our understanding of the role played by conserved hypothetical proteins in conjunction with divalent cations such as magnesium in regulating metabolic and virulence-related attributes of the agent of Lyme disease.

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Keywords

Borrelia burgdorferi, Genetics, Lyme disease, Magnesium

Citation

Department

Integrative Biology