Mentor: Dr. Jorg Bungert
College of Medicine
"I applied to the University Scholars program to enrich my undergraduate research experience at the University of Florida. As part of the University Scholars program, I hope to better develop my skills as a scientist by gaining knowledge in my field, mastering new techniques, and interacting closely with faculty members."
Florida Academic Scholar
HHMI Science for Life Undergraduate Research Award, 2011
President’s Honor Roll Spring 2010
Dean’s List Fall 2009- Spring 2012
Hobbies and Interests
The Role of HMGA-1 on Pol II Binding at the Beta-Globin Promoter
Enhancer regions are regulatory DNA sequences that control gene expression over long distances. Mutations in enhancer elements likely contribute to many diseases in the human population, due to down regulation of specific gene products. The human beta-globin gene represents a model system to study enhancer elements. Mutations in the beta-globin enhancer have been shown to lead to blood based diseases, such as sickle-cell anemia. The beta-globin enhancer region, known as the Locus Control Region (LCR) is made up of five different regions of DNA, called Hypersensitive Sites (HS), with each HS being numbered 1-5. Transcription complexes are proteins that bind to the beginning of genes and transcribe DNA into RNA, which serves as a template for protein synthesis. At the beta-globin locus, the transcription complex Pol II is recruited first to the LCR. A looping of the DNA then occurs, which brings the LCR closer to the beta-globin promoter, a regulatory DNA region that is directly upstream of the gene itself. Pol II is then recruited to the promoter region, from HS2 and transcription begins. The protein HMGA-1 has been shown to mediate transcription complex recruitment at the beta-globin promoter from HS2. It is hypothesized that knockdown of HMGA-1 will cause the beta-globin promoter to be unable to take Pol II from HS2, resulting in increased Pol II at HS2 and decreased Pol II at the beta-globin promoter, and thus decreased transcription of beta-globin.