Biology Professor and Research Students` Paper is Published

Associate Professor Marcy Kelly, PhD, Jessica Shepard ě°˝€™08 and Anangely Bello ě°˝€™07

– (from left to right) Associate Professor Marcy Kelly, PhD, Jessica Shepard ‘08 and Anangely Bello ‘07

Marcy Kelly, PhD, Associate Professor and Assistant Chair, Biology and Health Sciences (NYC), and her team of student researchers had their paper, “A triclosan-ciprofloxacin cross-resistant mutant strain of Staphylococcus aureus displays an alteration in the expression of several cell membrane structural and functional genes,” published in the peer-reviewed journal Research in Microbiology in the October-November 2007 issue. Student co-authors include:

  • Anangely Bello ‘07 (working in a research lab at Columbia University)
  • Amy Joy ‘07 (working at the Medical Examiners office, Boston)
  • Indira Londono ‘07 (working in a research lab at Columbia University)
  • Jehona Marku ‘06 (working as a Physician Assistant)
  • Jessica Shepard ‘08 (applying to graduate school)
  • Olga Tkachenko ‘05 (working towards a PhD at Cornell University)

Paper Abstract:

Triclosan is an antimicrobial agent found in many consumer products. Triclosan inhibits the bacterial fatty acid biosynthetic enzyme, enoyl-ACP reductase (FabI). Decreased susceptibility to triclosan correlates with ciprofloxacin resistance in several bacteria. In these bacteria, resistance to both drugs maps to genes encoding multi-drug efflux pumps. The focus of this study was to determine whether triclosan resistance contributes to ciprofloxacin resistance in Staphylococcus aureus. In S. aureus, triclosan resistance maps to a fabI homolog and ciprofloxacin resistance maps to genes encoding DNA gyrase, topoisomerase IV and to the multi-drug efflux pump, NorA. Using a NorA overexpressing mutant, we demonstrated that upregulation of NorA does not lead to triclosan resistance. To further investigate triclosan/ciprofloxacin resistance in S. aureus, we isolated triclosan/ciprofloxacin-resistant mutants. The mutants were screened for mutations in the genes encoding the targets of triclosan and ciprofloxacin. One mutant, JJ5, was wild-type for all sequences analyzed. We next monitored the efflux of triclosan from JJ5 and determined that triclosan resistance in the mutant was not due to active efflux of the drug. Finally, gene expression profiling demonstrated that an alteration in cell membrane structural and functional gene expression is likely responsible for triclosan and ciprofloxacin resistance in JJ5.

Read the paper