Presentation Title

On the Mechanism of Action of Antitoxoplasma Compound SW33

Presenter Information

Sean WatsonFollow

Advisor Information

Paul Davis, Ph.D.

Location

Room 112

Presentation Type

Oral Presentation

Start Date

1-3-2019 10:30 AM

End Date

1-3-2019 11:45 AM

Abstract

ON THE MODE OF ACTION OF ANTITOXOPLASMA COMPOUND SW33

Sean Watson, Austin Sanford, and Paul Davis, Department of Biology, University of Nebraska at Omaha.

As antimicrobial drug resistance continues to increase throughout the world, there lies an urgent need for the development of novel, efficacious drug treatments. As antimicrobial drugs are developed, their mode of action (MOA) is often identified before they become potential candidates for clinical use. Determining the MOA is important as it demonstrates the function of the drug at the cellular level and exposes potential risks for toxicity. One method to determine the MOA, termed chemical mutagenesis, consists of the induction of drug resistance in vitro followed by examination of the resistant population’s genomes to identify which genes are conferring resistance. In this work, I utilize the ubiquitous parasite Toxoplasma gondii to explore a novel method of double mutagenesis with the goal of determining the MOA of experimental compound SW33, a drug that has shown efficacy against both T. gondii and the causative agent of malaria, Plasmodium falciparum.

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Mar 1st, 10:30 AM Mar 1st, 11:45 AM

On the Mechanism of Action of Antitoxoplasma Compound SW33

Room 112

ON THE MODE OF ACTION OF ANTITOXOPLASMA COMPOUND SW33

Sean Watson, Austin Sanford, and Paul Davis, Department of Biology, University of Nebraska at Omaha.

As antimicrobial drug resistance continues to increase throughout the world, there lies an urgent need for the development of novel, efficacious drug treatments. As antimicrobial drugs are developed, their mode of action (MOA) is often identified before they become potential candidates for clinical use. Determining the MOA is important as it demonstrates the function of the drug at the cellular level and exposes potential risks for toxicity. One method to determine the MOA, termed chemical mutagenesis, consists of the induction of drug resistance in vitro followed by examination of the resistant population’s genomes to identify which genes are conferring resistance. In this work, I utilize the ubiquitous parasite Toxoplasma gondii to explore a novel method of double mutagenesis with the goal of determining the MOA of experimental compound SW33, a drug that has shown efficacy against both T. gondii and the causative agent of malaria, Plasmodium falciparum.