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SUMMER UNDERGRADUATE RESEARCH PROGRAMS
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Dr. James Morris

 

  

Jim Morris

  

Assistant Professor of Genetics and Biochemistry
Ph.D., Cellular Biology, 1997 University of Georgia

Research Interests
Molecular and Biochemical Parasitology
Molecular Surface Molecule Expression in Trypanosomes

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

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.

  

Trypanosome Research

Confocal Microscopy
of
Trypanosoma brucei

 

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.
 

 
  SELECTED PUBLICATIONS
 

 

  

Sevapandiyan, A, Kumar, P, Morris, JC, Salisbury, JL, Wang, CC, and Hakhasi, HL.  Centrin1 is required for organelle segregation and cytokinesis in Trypanosoma brucei.  (2007)  Molecular Biology of the Cell  In Press.

Morris, JC, Morris, MT, Lee, SY, Toole, WP, Seifert, CM, and Acosta-Serrano, A. Chapter 3 – Reverse and forward genetics as practical approaches for post-genome studies. In: Barry, D., Mottram, J., McCulloch, R., Acosta-Serrano, A., eds.  Trypanosomes -After the Genome. Horizon Bioscience, 2007.  49-70.

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

Drew, ME, Motyka, SA, Morris, JC, Wang, Z, and Englund, PT.  Inducible RNAi as a forward genetic tool in Trypanosoma brucei.  In: Appasani, K, editor.  RNA Interference:  From Basic Science to Drug Development.  Cambridge:  Cambridge University Press. 2005.  247-256.

Morris, JC, Wang, Z, Motyka, SA, Drew, ME, and Englund, PT.  "An RNAi-based genomic library for forward genetics in the African trypanosome.  In: Sohail, M, editor.  Gene Silencing by RNA Interference: Technology and Application. Boco Raton:  CRC Press LLC, 2004.  241-257.

Leal, S, Acosta-Serrano, A, Morris, JC. and Cross, GAM.  Transposon mutagenesis of Trypanosoma brucei identifies glycosylation mutants resistant to concanavalin A. (2004) The Journal of Biological Chemistry 279, 28979-28988. 

Drew ME*, Morris, JC*, Wang, Z*, (*All Contributed Equally), Wells, L, and Englund, PT.  The adenosine analog tubercidin inhibits glycolysis in Trypanosoma brucei as revealed by an RNAi library. (2003) The Journal of Biological Chemistry 278, 46596-46600. 

Morris, JC*, Wang, Z*, Drew, ME*, (*All Contributed Equally), and Englund, PT.  Glycolysis modulates trypanosome glycoprotein expression as revealed by an RNAi library. (2002) The EMBO Journal 21, 4429-4438.
   
 

 
Interim Chair: Dr. Albert Abbott

100 Jordan Hall
Clemson, SC 29634-0318
Tel: (864) 656-6237
Fax: (864) 656-6879
    
 
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