"I applied to the University Scholars Program to amplify and truly benefit from my research experience at the University of Florida. The process of submitting a proposal, regularly updating a research portfolio and presenting findings at a forum of peers will not only consolidate and complement my in-lab work at UF but also prepare me well for handling and working with research in the future, especially in my chosen field of medicine. I hope to gain a mastery of basic molecular biological and microbiological laboratory and analysis techniques, and in particular become proficient at working with and analyzing mutations in bacterial and eukaryotic DNA at a basic level. This year, I hope to maintain good grades, score well on the MCAT, and successfully complete the research objectives I have set out to fulfill."
Microbiology and Cell Science
I am a Microbiology and Cell Sciences major, and I have always been academically interested in the genetics of microbes and their pathogenic potential. However, my primary research interest--analysis of DNA repair mechanisms in eukaryotes--falls under the purview of molecular biology, although my lab still uses bacteria as model organisms. As part of my primary research project, I am learning to 1) produce specific plasmids using bacteria; 2) modify plasmids by adding the appropriate lesions; 3) run transcription assays on these plasmids using eukaryotic protein extracts; and 4) analyze the results of these assays to investigate the overall repair mechanism.
Academic and Other Awards
- University Scholars Program Scholarship (2011-2012)
- Dean's List
- Florida Bright Futures
- Heal the World
- UF Campus Kitchens
Shands Hospital Volunteer: Pharmacy Interface Youth Mentoring UF Campus Kitchens.
Hobbies and Interests
- Running, biking, swimming, piano, flute, reading, music, and history.
The Mechanism of Eukaryotic Transcription-Coupled Repair At Abasic Sites
Abasic sites, also known as AP (apurinic/apyrimidinic) sites, are a common type of DNA lesion that is produced when the bond between the sugar and base of a nucleotide is cleaved, releasing the base. They occur through DNA damage or as an intermediate step in base excision repair. Left unrepaired, AP sites block transcription in prokaryotes and eukaryotes by stalling the transcribing RNA polymerase (RNAP) at the lesion site. Indefinite blockage is a signal for apoptosis. Nucleotide excision repair (NER) reverses a lesion by excising it and filling in the gap using the complementary undamaged strand as the template. A sub-pathway of NER is transcription-coupled repair (TCR). TCR requires an RNAP stalled at a lesion in the transcribed strand, and seeks to restore transcription by removing the stalled RNAP and recruiting NER repair proteins to the lesion. The mechanism of TCR has been well understood in bacteria, but is poorly understood in eukaryotes. We propose to study the mechanism of AP site TCR in eukaryotes. We hypothesize that after RNAP arrest and repair at the lesion, transcription will restart and continue past the repaired lesion site. An AP site will be introduced into a plasmid containing a ribozyme sequence at a known site downstream from the lesion. We will use monoclonal antibodies against RNA to prepare purified RNAPs arrested at AP sites, and incubate them with HeLa (eukaryotic) protein extracts. We will then measure any subsequent transcriptional restart and repair synthesis via transcript length analysis and other procedures used routinely in our laboratory. Learning the mechanism of TCR at AP sites has significant implications for the explanation of some of the phenotypic manifestations of TCR-deficient human diseases such as Cockayne syndrome, which is characterized by neurodegradation, developmental defects and premature aging.