Dr. James Morris

Associate Professor
Ph.D. Cellular Biology
1997, University of Georgia

Research Interests
Molecular and Biochemical Parasitology
Surface Molecule Expression in Trypanosomes

Office: 214 Biosystems Research Complex
Phone: (864) 656-0293
Email: jmorri2@clemson.edu
Website: http://www.morrislabs.com/

Research Activities

The African trypanosome, Trypanosoma brucei, is the single-celled parasite that causes the devastating diseases African sleeping sickness in man and nagana in cattle. Because of the lack of suitable anti-trypanosomal treatments, these diseases impact the health and nutritional well-being of millions of people in sub-Saharan Africa. Trypanosomiasis causes greater mortality than HIV/AIDS in some areas of Africa and is currently considered an uncontrolled disease by the World Health Organization.

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.

T. 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 b 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.

Research on the Radio

Hear about Morris Lab research on the Radio.

Recent Publications

Clemmens CS, Morris MT, Lyda TL, Acosta-Serrano, A, Morris JC. Trypanosoma brucei AMP-Activated Kinase Subunit Homologs Influence Surface Molecule Expression. (In Press) Experimental Parasitology

Chambers, JW, Kearns, M, Morris MT, Morris JC. Assembly of heterohexameric trypanosome hexokinases reveals that hexokinase 2 is a regulable enzyme. (2008) The Journal of Biological Chemistry 283, 14963-70.

Chambers, JW, Fowler, ML, Morris MT, Morris JC. The anti-trypanosomal agent lonidamine inhibits Trypanosoma brucei hexokinase 1, (2008) Molecular and Biochemical Parasitology 158, 202-207.

Chambers, JW, Morris, MT, Smith, KS and Morris, JC. Residues in an ATP binding domain influence sugar binding in a trypanosome hexokinase. (2008) Biochemical and Biophysical Research Communications 365(3), 420-5.

Morris, MT, DeBruin, C, Yang, Z, Chambers, JW, Smith, KS and Morris, JC. Activity of a second Trypanosoma brucei hexokinase is controlled by an 18 amino acid C-terminal tail. (2006) Eukaryotic Cell 5, 2014-2023.

Additional Publication Resources