Date of Award

Spring 5-2017

Degree Type

Honors College Thesis

Department

Biological Sciences

First Advisor

Mohamed Elasri

Advisor Department

Biological Sciences

Abstract

Persister cells comprise a phenotypic variant that shows extreme antibiotic tolerance resulting in chronic infections. While this phenomenon has posed a great threat in public health, mechanism underlying their formation in Staphylococcus aureus remains largely unknown. Increasing evidence of the presence of persister cells in recalcitrant infections underscores the great urgency to unravel the mechanism by which these cells are developed. The Elasri Research group characterized msaABCR operon that plays roles in regulation of virulence, biofilm development and antibiotic resistance. It was hypothesized that the operon also plays a role in persister cell formation. In this study, the persister cell fraction in wild type (WT) USA300 LAC, its isogenic msaABCR deletion mutant (ΔmsaABCR) and complemented operon mutant (complement) strains were compared. The present study shows that the ΔmsaABCR forms fewer persister cells as compared to WT challenged with various antibiotics single as well as in the combinations in exponential as well as in the stationary phase. The complement restored the phenotype as comparable to the WT in most of the drug tested. Likewise, the ΔmsaABCR also formed less number of persister cells challenged with gentamycin in the presence of metabolite fructose. Taken together, this study suggests that msaABCR plays role in the persister formation. Ultimately, the goal is to define the mechanism that causes msaABCR to control persistence. This study will bring new insights into the understanding of persister cells formation and consequently overcome failures of staphylococcal infections.

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