SARAH WU

Antibiotic resistant pathogens are a direct result of the adaptive nature of evolution. The presence of antibiotic resistance in clinical and agricultural settings presents a dilemma concerning the use and development of new antibiotics. Once an antibiotic is introduced, it is only a matter of time before strains become resistant. Since the inception of antibiotic treatments in the clinical setting, the rate of antibiotic resistance is rising with the increased usage of antibiotics, while the development of new antibiotics has decreased. We are using experimental evolution to develop and model the mechanisms of adaptation. To resist beta-lactam antibiotics, E. coli employs the enzyme beta-lactamase, which hydrolyzes the antibiotic, rendering it inactive. Certain mutations in the TEM-1 (beta-lactamase) gene allow the bacteria to be able to hydrolyze an increased variety of beta-lactam antibiotics and thus improve its chances for survival. To explore this issue, E. coli strains transformed with drug resistance plasmid pBR322 were subjected to increasing dosage and constant exposure to the beta-lactam drug cefotaxime to select for beneficial mutations. We hope to map out the evolutionary trajectories of the TEM-1 gene that lead to increased resistance in order to better understand drug resistance and molecular evolution.

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