James C. Morris


Email: jmorri2@clemson.edu
Office: 656-0293

Department of Genetics and Biochemistry

LSF 249

Ph.D., University of Georgia, 1997
M.S., University of Georgia, 1992
B.S., College of William and Mary, 1990

Research interest:
Parasites that have developmental stages in distinct hosts encounter remarkably different environments during their lifecycles. For example, parasite members of the family Trypanosomatidae, including the African and American trypanosomes and Leishmainia spp., have required lifecycle stages in both insect vector and mammalian host. These parasites have evolved distinct mechanisms to avoid eradication by the host immune system. In common, however, is the requirement that these parasites must be able to identify the host in which they reside and respond accordingly. The African trypanosome, Trypanosoma brucei, responds to changes in environmental glucose availability to regulate developmental progression. While in the mammalian blood, the parasite is bathed in glucose at a nearly constant concentration (~5 mM). Shortly after ingestion by a feeding tsetse fly, the blood sugar is depleted, triggering a developmental program in the parasite. While glucose sensing is not unique to T. brucei (pancreatic cells respond to blood glucose levels by the release of insulin in order to maintain homeostasis in mammals), the parasites have evolved the means to “sense” dramatic changes in the environment (from mammal to insect). Our group is interested in elucidating the molecular mechanisms employed by the African trypanosome to detect glucose availability, with a particular focus on identifying unique components for targeting for therapeutics. Rationale: The parasitic members of the family Trypanosomatidae infect ~32 million people worldwide. The lack of effective therapies for these maladies emphasizes the need for the identification of new targets for drug development. Our research focuses on identifying for the development of therapies the mechanisms that the African trypanosome uses to “sense” its environment and make developmental decisions.

Joice, AC, Harris, MT, Kahney, EK, Dodson, HC, Maselli, AG, Whitehead, DC, and Morris JC. Exploring the mode of action of ebselen in Trypanosoma brucei hexokinase inhibition. (2013) The International Journal for Parasitology: Drugs and Drug Resistance 3, 154-160. (*Selected as “Editor’s Choice”)
Bauer, ST, Morris, JC, Morris, MT. Environmentally-regulated glycosome protein composition in the African trypanosome. (2013) Eukaryotic Cell 12, 1072-1079.
Harris, MT, Walker, DM, Drew, ME, Mitchell, WG, Dao, K, Schroeder, CE, Flaherty, DP, Weiner, WS, Golden JE, and Morris, JC. Interrogating a Hexokinase-Selected Small Molecule Library for Inhibitors of Plasmodium falciparum Hexokinase. (2013) Antimicrobial Agents and Chemotherapy 57, 3731-3737.
Lin, S, Morris, MT, Ackroyd, CP, Morris, JC, Christensen, KA. Peptide targeted delivery of pH sensor for quantitative measurements of intraglycosomal pH in live Trypanosoma brucei. (2013) Biochemistry 52, 3629-3637.
Joice, AC, Lyda, TL, Sayce, AC, Verplaetse, E, Morris, MT, Michels, PAM, Robinson, DR, Morris, JC. Extra-glycosomal localization of Trypanosoma brucei Hexokinase 2. (2012) The International Journal for Parasitology 42,401-409. (*Selected as “Editor’s Choice”)