Jennifer Güler

Assistant Professor of Biology
214 PLSB  
(434) 982-5481

Education

  • B.S., University of California, Santa Barbara, 2000
  • Ph.D., Johns Hopkins Medical Institute, 2007
  • Postdoc, Johns Hopkins Medical Institute, 2007-2008
  • Postdoc, University of Washington, 2008-2013

Research Interests

Research in the Güler Malaria Lab focuses on the human-infective malaria parasite, Plasmodium falciparum. Some of our projects are described below:

·         We are interested in underlying mechanisms that drive genetic change in parasites during the development of antimalarial resistance. Our studies in this area utilize a range of cellular, biochemical and molecular techniques to uncover pathways that are important for this process.

·         Some genetic alterations that arise during antimalarial exposure drive metabolic adaptation in the parasite. By employing metabolite profiling paired with computational modeling to investigate these slight adjustments, we aim to reveal unique pathways that enhance parasite survival.

·         We partner with researchers in malaria endemic countries to apply our predictions from lab-based models to investigations with patient-isolated parasites. These studies inform our knowledge of general parasite adaptation and its effect on disease severity.  For more information, please visit the Güler Malaria Lab Website.

Representative Publications

  • Pholwat, S., Liu, J., Stroup, S., Jacob, S., Banura, P., Moore, C., Huang, F., Laufer, M., Houpt, E., Güler, J. The Malaria TaqMan Array Card: 87 assays for Plasmodium falciparum drug resistance, speciation, and genotyping in a single reaction.. Antimicrob Agents Chemother. 2017 Mar 6. pii: AAC.00110-17. doi:10.1128/AAC.00110-17.
     
  • Güler, J.L., White, J., Phillips, M.A., Rathod, P.K. (2015). Atovaquone tolerance in Plasmodium falciparum parasites selected for high level resistance to a dihydroorotate dehydrogenase inhibitor. Antimicrobial Agents and Chemotherapy, 59(1):686-9. PMCID:PMC4291421.
     
  • Güler, J.L., Freeman, D.L., Ahyong, V., Patrapuvich, R., White, J., Gujjar, R., Phillips, M.A., Derisi J., Rathod, P.K. (2013). Asexual populations of the human malaria parasite, Plasmodium falciparum, use a two-step genomic strategy to acquire accurate, beneficial DNA amplifications. PLoS Pathogens, 9(5):e1003375. PMID: 23717205.
     
  • Narayanasamy, K., Chery, L., Basu, A., Duraisingh, M.T., Escalante, A., Fowble, J., Güler, J.L., Herricks, T., Kumar, A., Majumder, P., Maki, J., Mascarenhas, A., Rodrigues, J., Roy, B., Sen, S., Shastri, J., Smith, J., Valecha, N., White, J., Rathod, P.K. (2012). Malaria evolution in South Asia: knowledge for control and elimination. Acta Tropica, 121(3):256-66. PMID: 22266213.
     
  • Clayton, A.M.*, Güler, J.L.*, Lindsay, M.E.*, Gluenz, E., Gull, K., Smith, T., Jensen, R.E., Englund, P.T. (2011). Depletion of mitochondrial acyl carrier protein in bloodstream-form Trypanosoma brucei causes a kinetoplast segregation defect. Eukaryotic Cell, 10(3):286-92. PMID: 21239625 (*) denotes triple first authorship.
     
  • Autio K.J., Güler J.L., Kastaniotis A.J., Englund P.T., Hiltunen J.K. (2008). The 3-hydroxyacyl-ACP dehydratase of mitochondrial fatty acid synthesis in Trypanosoma brucei. FEBS Letters, 582(5):729-33. PMID: 18258193.
     
  • Güler J.L., Protivínská E., Smith T.K., Lukeš J., Englund P.T. (2008). Mitochondrial fatty acid synthesis is required for normal mitochondrial function and morphology in Trypanosoma brucei. Molecular Microbiology, 67(5):1125-42. PMID: 18221265.