Student Author Information

Jody Caretti, University of LynchburgFollow

Location

Schewel 232

Access Type

Open Access

Presentation Type

Oral Presentation

Start Date

April 2022

Department

Biology

Abstract

Widespread antibiotic resistance has quickly become one of the most concerning crises affecting modern medicine, especially in cases of Staphylococcal infections, which have become resistant to all ��-lactam antibiotics. As a result, research into alternative forms of treatment for bacterial infections is a top priority. Bacteriophage therapy is a popular candidate for replacing antibiotics, due to the way the viruses interact with the bacteria. The 80�� prophage integrates its DNA into Staphylococcus aureus strain 10616 via the lysogenic cycle, and replicates with the bacterial cell. When stressed, the bacteria stop replicating and the prophage stimulates the lytic cycle, activating transcription in order to reproduce and release progeny phages, consequently killing the bacterial cell. Preliminary data has indicated that there is a secondary transcription start site of this prophage DNA that, when activated, could prevent the packaging of the viral DNA into progeny viruses, while still causing cell lysis to occur. This would, in theory, prevent further spread of the virus, but would still kill the infectious bacteria. Using the preliminary data, we investigated the location of this alternative transcription start site within the integrated prophage DNA.

Faculty Mentor(s)

Dr. Jamie Brooks

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Apr 6th, 9:15 AM

Investigating alternative induction of the S. aureus 80a prophage

Schewel 232

Widespread antibiotic resistance has quickly become one of the most concerning crises affecting modern medicine, especially in cases of Staphylococcal infections, which have become resistant to all ��-lactam antibiotics. As a result, research into alternative forms of treatment for bacterial infections is a top priority. Bacteriophage therapy is a popular candidate for replacing antibiotics, due to the way the viruses interact with the bacteria. The 80�� prophage integrates its DNA into Staphylococcus aureus strain 10616 via the lysogenic cycle, and replicates with the bacterial cell. When stressed, the bacteria stop replicating and the prophage stimulates the lytic cycle, activating transcription in order to reproduce and release progeny phages, consequently killing the bacterial cell. Preliminary data has indicated that there is a secondary transcription start site of this prophage DNA that, when activated, could prevent the packaging of the viral DNA into progeny viruses, while still causing cell lysis to occur. This would, in theory, prevent further spread of the virus, but would still kill the infectious bacteria. Using the preliminary data, we investigated the location of this alternative transcription start site within the integrated prophage DNA.