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Science 4 June 2004:
Vol. 304. no. 5676, pp. 1515 - 1518
DOI: 10.1126/science.1098371
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Reports

A Process for Controlling Intracellular Bacterial Infections Induced by Membrane Injury

Deepannita Roy,1 David R. Liston,1* Vincent J. Idone,1 Anke Di,2 Deborah J. Nelson,2 Céline Pujol,3 James B. Bliska,3 Sabyasachi Chakrabarti,1 Norma W. Andrews1{dagger}

Strategies for inhibiting phagolysosome fusion are essential for the intracellular survival and replication of many pathogens. We found that the lysosomal synaptotagmin Syt VII is required for a mechanism that promotes phagolysosomal fusion and limits the intracellular growth of pathogenic bacteria. Syt VII was required for a form of Ca2+-dependent phagolysosome fusion that is analogous to Ca2+-regulated exocytosis of lysosomes, which can be triggered by membrane injury. Bacterial type III secretion systems, which permeabilize membranes and cause Ca2+ influx in mammalian cells, promote lysosomal exocytosis and inhibit intracellular survival in Syt VII +/+ but not –/– cells. Thus, the lysosomal repair response can also protect cells against pathogens that trigger membrane permeabilization.

1 Section of Microbial Pathogenesis and Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06510, USA.
2 Department of Pharmacology and Physiology, The University of Chicago, Chicago, IL 60637, USA.
3 Department of Molecular Genetics and Microbiology, Center for Infectious Diseases, School of Medicine, State University of New York at Stony Brook, Stony Brook, NY, 11794, USA.



* Present address: Regulatory Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.

{dagger} To whom correspondence should be addressed.

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