Presentation Type

Poster

Abstract

Borrelia burgdorferi, the bacterium that causes Lyme disease, is maintained in nature through an enzootic cycle, transiting between a mammalian host and tick vector. Following acquisition by a tick, B. burgdorferi uses the sugar glucose from the blood meal to survive. When this source of carbon runs out, the bacterium undergoes a state of nutrient stress. During this time, it uses the sugar glycerol as an alternate carbon and energy source. The glp operon is composed of three annotated genes that enable B. burgdorferi to import and metabolize glycerol. glpD, the last gene in the operon, encodes the enzyme glycerol-3-phosphate dehydrogenase that shuttles glycerol into glycolysis, the main pathway in the bacterium for extracting energy. The glpD gene is regulated differently than the other genes in the glp operon, which respond to nutrient stress, so I hypothesize that glpD is required for B. burgdorferi to use glycerol in both the tick and the mammal. Therefore, I have taken a genetic approach to test the role of glpD in survival of the bacterium and have constructed a mutant of B. burgdorferi lacking the glpD gene. My preliminary results suggest that the glpD mutant does not utilize glycerol as well as wild-type B. burgdorferi. I am currently generating a complement of this mutant to use as a control, and I will assay the phenotype of both the mutant and the complement for their ability to grow in glucose and glycerol. Eventually, I will test the mutant for its ability to survive in ticks and mice using the tick-murine model of Lyme disease.

Category

Life Sciences

Available for download on Saturday, September 30, 2017

Share

COinS
 
Apr 15th, 11:00 AM Apr 15th, 12:00 PM

The role of glycerol metabolism in the Lyme disease agent

Borrelia burgdorferi, the bacterium that causes Lyme disease, is maintained in nature through an enzootic cycle, transiting between a mammalian host and tick vector. Following acquisition by a tick, B. burgdorferi uses the sugar glucose from the blood meal to survive. When this source of carbon runs out, the bacterium undergoes a state of nutrient stress. During this time, it uses the sugar glycerol as an alternate carbon and energy source. The glp operon is composed of three annotated genes that enable B. burgdorferi to import and metabolize glycerol. glpD, the last gene in the operon, encodes the enzyme glycerol-3-phosphate dehydrogenase that shuttles glycerol into glycolysis, the main pathway in the bacterium for extracting energy. The glpD gene is regulated differently than the other genes in the glp operon, which respond to nutrient stress, so I hypothesize that glpD is required for B. burgdorferi to use glycerol in both the tick and the mammal. Therefore, I have taken a genetic approach to test the role of glpD in survival of the bacterium and have constructed a mutant of B. burgdorferi lacking the glpD gene. My preliminary results suggest that the glpD mutant does not utilize glycerol as well as wild-type B. burgdorferi. I am currently generating a complement of this mutant to use as a control, and I will assay the phenotype of both the mutant and the complement for their ability to grow in glucose and glycerol. Eventually, I will test the mutant for its ability to survive in ticks and mice using the tick-murine model of Lyme disease.