Jennifer Hewlett

 Jennifer Hewlett
Mentor: Dr. Kelly Rice
College of Agricultural and Life Sciences
 
"I initially became involved in research because I was curious; I wanted a different perspective on the material that I was learning in my microbiology courses. However, research gave me much more than a new perspective, it gave me a new way of thinking. While I've become skilled at new microbiological techniques such as phage transduction and allele-replacement mutagenesis, I've also become skilled at critical thinking, being patient and having discipline. My initial reasons for becoming involved in research are completely overshadowed by the research experience itself. The skills that I've learned during my time in research lab will aid me not only in my undergraduate course work, but also in my future medical school course work, and in my life."

Major

Microbiology and Cell Science

Minor

French and Francophone Studies

Research Interests

  • Microbiology
  • Genetics
  • Medicine

Academic Awards

  • N/A

Organizations

  • Golden Key International Honor Society
  • Phi Kappa Phi Honor Society

Volunteer

  • Shands Pediatric Emergency Department
  • Shands Occupational Therapy
  • UF Relay for Life

Hobbies and Interests

  • Watching Movies
  • Cooking
  • Reading
  • Traveling

Research Description

The role of ScdA in Staphylococcus aureus biofilm
Staphylococcus aureus is the perpetrator of numerous human illnesses, many of which are due to biofilm formation. Unpublished data from our lab has shown that nitric oxide (NO), a reactive radical gas, plays a role in S. aureus biofilm formation. Based on work done in Psuedomonas aeruginosa (Barraud et al., 2006), it is thought that many bacteria such as S. aureus endogenously produce NO as a regulator of cell death and dispersal, but not much is known of the molecular mechanism. How S. aureus cells can withstand so much nitrosative stress without perishing is a concern for our research lab and for public health. Through the study of ScdA, a di-iron S. aureus protein involved in protecting the bacteria from NO damage (Overton et al., 2007), I hope to elucidate one of the many ways in which this bacterium evades death. I also hope to investigate the role of ScdA in NO signaling. Other research labs have studied a ScdA homolog, the YftE protein in E. coli, and discovered that it has a non-heme iron center, a possible site for NO chemistry (Todorovic et al., 2008, Justino et al., 2007), and that the protein is essential to E. coli’s restoration of iron-sulfur clusters that have been damaged by nitrosative stress (Justino et al., 2007). Based on these findings, it seems that if scdA is absent from the genome, cells will lose the ability to repair iron-sulfur protein centers that have been damaged by NO production. If ScdA can also scavenge NO, a scdA mutant may also display increased NO levels. The first step towards revealing the role of ScdA in biofilm formation is through the determination of its biofilm phenotype. I will accomplish this by comparing the viability and biofilm structure of a scdA mutant to wild type and complement strains through the use of a fluorescent LIVE/DEAD stain, which differentiates living from dead cells. Additionally, I plan to observe the different phenotypes between these two groups when treating the biofilms with NO in order to determine the scdA mutant’s proficiency in managing nitrosative stress. NO signaling will be observed through the use of DAF-FM, a stain that reacts with NO to produce visible fluorescence in a biofilm.