The Journal of Experimental Medicine
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Published online 7 May 2001.
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© The Rockefeller University Press, 0022-1007/2001/5/1097/ $5.00
The Journal of Experimental Medicine, Volume 193, Number 9, May 7, 2001 1097-1104

Brief Definitive Report

The Exocytosis-regulatory Protein Synaptotagmin VII Mediates Cell Invasion by Trypanosoma cruzi

Elisabet V. Calera, Sabyasachi Chakrabartia, Kimberly T. Fowlera, Swathi Raoa, and Norma W. Andrewsa
a Section of Microbial Pathogenesis, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06520

Correspondence to: Norma W. Andrews, Section of Microbial Pathogenesis, Boyer Center for Molecular Medicine, Yale University School of Medicine, 295 Congress Ave., New Haven, CT 06536. Tel:203-737-2410 Fax:203-737-2630 E-mail:norma.andrews{at}yale.edu.

The intracellular protozoan parasite Trypanosoma cruzi causes Chagas' disease, which affects millions of people in Latin America. T. cruzi enters a large number of cell types by an unusual mechanism that involves Ca2+-triggered fusion of lysosomes with the plasma membrane. Here we show that synaptotagmin VII (Syt VII), a ubiquitously expressed synaptotagmin isoform that regulates exocytosis of lysosomes, is localized on the membranes of intracellular vacuoles containing T. cruzi. Antibodies against the C2A domain of Syt VII or recombinant peptides including this domain inhibit cell entry by T. cruzi, but not by Toxoplasma gondii or Salmonella typhimurium. The C2A domains of other ubiquitously expressed synaptotagmin isoforms have no effect on T. cruzi invasion, and mutation of critical residues on Syt VII C2A abolish its inhibitory activity. These findings indicate that T. cruzi exploits the Syt VII–dependent, Ca2+-regulated lysosomal exocytic pathway for invading host cells.

Key Words: trypanosome, parasite, intracellular, secretion, calcium


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