|
|
|
|
|
||
|
|||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | |||||
Journal of Cell Science, Vol 106, Issue 4 1023-1033, Copyright © 1993 by Company of Biologists
JOURNAL ARTICLES |
AR de Jesus, R Cooper, M Espinosa, JE Gomes, ES Garcia, S Paul and GA Cross
Laboratory of Molecular Parasitology, Rockefeller University, New York, NY 10021.
We have explored the biological function of a surface glycoprotein (GP72) of Trypanosoma cruzi by studying a null mutant parasite, generated by targeted gene deletion. GP72 deletion affected parasite morphology in several stages of the life cycle. Insect midgut (epimastigote) forms had a detached flagellum (apomastigote) in the null mutant. The abnormal flagellar phenotype persisted during development of the infective (metacyclic) forms but there was no impairment in the acquisition of complement resistance, sialidase expression or cell infectivity. The GP72 null mutant could efficiently infect and proliferate in mouse macrophages and non-phagocytic L6E9 cells. The mammalian stages of the life cycle also showed major morphological abnormalities. During early subcultures in L6E9 cells, few extracellular fully flagellated forms, expressing markers characteristic of trypomastigotes, were seen. The extracellular population consisted almost exclusively of rounded forms with short flagella (micromastigote), which expressed an amastigote-specific surface marker and no sialidase. The propagation of the parasite was not affected, despite the apparent lack of the trypomastigote forms, which are thought to be primarily responsible for cell invasion. After some subcultures, the extracellular population changed to about equal numbers of micromastigotes and a range of flagellated forms that still did not include true trypomastigotes. Instead, the kinetoplast remained close to the nucleus and the flagellum emerged from the middle of the cell (mesomastigote). Half of the flagellum adhered to the cell body and the remainder was free at the anterior end. In Triatoma infestans, the survival of the mutant was dramatically reduced, suggesting that either GP72 itself, or the altered properties of the flagellum, were critical for establishment in the insect vector.
This article has been cited by other articles:
|
|
 |
|
  M. P. Zago, A. B. Barrio, R. M. Cardozo, T. Duffy, A. G. Schijman, and M. A. Basombrio Impairment of Infectivity and Immunoprotective Effect of a LYT1 Null Mutant of Trypanosoma cruzi Infect. Immun., January 1, 2008; 76(1): 443 - 451. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. C. Turnock, L. Izquierdo, and M. A. J. Ferguson The de Novo Synthesis of GDP-fucose Is Essential for Flagellar Adhesion and Cell Growth in Trypanosoma brucei J. Biol. Chem., September 28, 2007; 282(39): 28853 - 28863. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. C. Turnock and M. A. J. Ferguson Sugar Nucleotide Pools of Trypanosoma brucei, Trypanosoma cruzi, and Leishmania major Eukaryot. Cell, August 1, 2007; 6(8): 1450 - 1463. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. L. Hill Biology and Mechanism of Trypanosome Cell Motility Eukaryot. Cell, April 1, 2003; 2(2): 200 - 208. [Full Text] [PDF]
|
|
|
|
|
|
D. J. LaCount, B. Barrett, and J. E. Donelson Trypanosoma brucei FLA1 Is Required for Flagellum Attachment and Cytokinesis J. Biol. Chem., May 10, 2002; 277(20): 17580 - 17588. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Vaidya, M. Bakhiet, K. L. Hill, T. Olsson, K. Kristensson, and J. E. Donelson The Gene for a T Lymphocyte Triggering Factor from African Trypanosomes J. Exp. Med., August 4, 1997; 186(3): 433 - 438. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Haynes, D. Russell, and G. Cross Subcellular localization of Trypanosoma cruzi glycoprotein Gp72 J. Cell Sci., January 12, 1996; 109(13): 2979 - 2988. [Abstract] [PDF]
|
|
