Year of Award

2015

Document Type

Thesis

Degree Type

Master of Science (MS)

Degree Name

Cellular, Molecular and Microbial Biology

Department or School/College

Division of Biological Sciences

Committee Chair

Scott Samuels

Committee Co-chair

Dan Drecktrah

Commitee Members

Stephen Lodmell, Bruce Bowler

Subject Categories

Microbiology | Molecular Genetics

Abstract

Borrelia burgdorferi, the bacterium that causes Lyme disease, is maintained in nature through an enzootic cycle that includes a tick vector and a vertebrate host. The bacterium is acquired by an Ixodes tick from an infected vertebrate. The bacterium alters its gene expression to adapt to different environments of the tick and vertebrate. Between tick feedings, B. burgdorferi must contend with nutrient stress. The stringent response is a physiological mechanism when bacteria switch from “thriving” to “surviving” mode in response to limited nutrient resources; it is mediated by an increase in the nucleotide alarmone guanosine penta- or tetraphosphate, abbreviated as (p)ppGpp. An important target of the stringent response is transcriptional regulation, which is mediated by the RNA polymerase-binding transcription factor DksA. We hypothesized that DksA potentiates the effects of the stringent response for B. burgdorferi during starvation, and regulates B. burgdorferi genes involved in tick persistence. We have taken a reverse genetic approach in which we have generated a dksA null mutant and the corresponding complemented strain. In vitro experiments indicate that DksA may play a role in growth, cell viability during starvation, and cell morphology. We also provide evidence that the presence of glycerol during starvation affects cell viability and morphology of B. burgdorferi.

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© Copyright 2015 Britney Cheff