期刊
SCIENCE
卷 304, 期 5676, 页码 1515-1518出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1098371
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资金
- NIAID NIH HHS [AI48507, AI43389, AI34867] Funding Source: Medline
- NIGMS NIH HHS [R01 GM064625, GM64625] Funding Source: Medline
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.
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