A Process for Controlling Intracellular Bacterial Infections Induced by Membrane Injury

Roy, Deepannita; Liston, David R.; Idone, Vincent; Di, Anke; Nelson, Deborah J.; Pujol, Céline; Bliska, James B.; Chakrabarti, Sabyasachi; Andrews, Norma W.

doi:10.1126/science.1098371

Cited by 131 publications

(129 citation statements)

References 22 publications

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“…Previous studies in fibroblasts demonstrated that genetic ablation of Syt VII inhibits lysosomal exocytosis, when the process is triggered by Ca 2ϩ influx at sites of membrane injury (Chakrabarti et al, 2003;Roy et al, 2004) or by mobilization of intracellular Ca 2ϩ stores through receptor-mediated agonists Jaiswal et al, 2004). In contrast, the higher and more widespread [Ca 2ϩ ] i elevation resulting from stimulation with Ca 2ϩ ionophores can also trigger lysosomal exocytosis in Syt VII-deficient cells, albeit with a markedly altered secretory pattern when compared with wild-type cells (Jaiswal et al, 2004).…”

Section: Neurite Outgrowth Is Impaired In Scg Neurons From Syt Vii-dementioning

confidence: 99%

A Role for Synaptotagmin VII-Regulated Exocytosis of Lysosomes in Neurite Outgrowth from Primary Sympathetic Neurons

Arantes¹,

Andrews²

2006

J. Neurosci.

143

131

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Neurite outgrowth is mediated by the exocytosis of intracellular vesicles at the tips of elongating neuronal processes. The lysosomal vesicle-associated soluble N-ethylmaleimide-sensitive factor attachment protein receptor tetanus neurotoxin insensitive vesicleassociated membrane protein (TI-VAMP)/VAMP7 was previously implicated in membrane fusion events mediating neurite outgrowth, but the participation of lysosomes in this exocytic process has remained unclear. Here, we show that VAMP7 and the lysosomal glycoprotein Lamp1 extensively colocalize in vesicles present throughout the soma and neurite outgrowths of primary sympathetic neurons. Synaptotagmin VII (Syt VII), a Ca 2ϩ -sensing synaptotagmin isoform previously shown to interact with VAMP7 during lysosomal exocytosis in fibroblasts, was detected on a subset of these lysosomal glycoprotein 1 (Lamp1)/VAMP7-positive neuronal vesicles. Ionophore-stimulated exocytosis triggered exposure of the luminal domains of both Lamp1 and Syt VII at overlapping sites on the neuronal surface, indicating that the Syt VII-containing lysosomal compartments fuse with the plasma membrane in response to [Ca 2ϩ ] i elevation. To determine whether Syt VII was required for the exocytic events mediating neurite extension, we followed the development of superior cervical ganglion neurons explanted from Syt VII-deficient mice. The results revealed a marked defect in neurite outgrowth and arborization, suggesting that Ca 2ϩ -dependent, Syt VII-regulated exocytosis of late endosomes/lysosomes plays a role in the addition of new membrane to developing neurite extensions.

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Section: Neurite Outgrowth Is Impaired In Scg Neurons From Syt Vii-dementioning

confidence: 99%

A Role for Synaptotagmin VII-Regulated Exocytosis of Lysosomes in Neurite Outgrowth from Primary Sympathetic Neurons

Arantes¹,

Andrews²

2006

J. Neurosci.

143

131

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“…Syt IV regulates glutamate release from astrocytes (30). Syt VI is involved in the Ca 2ϩ -dependent acrosome reaction in sperm cells (31), and Syt VII regulates Ca 2ϩ -dependent lysosomal exocytosis in fibroblasts (32)(33)(34)(35).…”

Section: Synaptotagmin (Syt)mentioning

confidence: 99%

Synaptotagmin VII Is Targeted to Dense-core Vesicles and Regulates Their Ca2+-dependent Exocytosis in PC12 Cells

Fukuda

Kanno

Satoh

et al. 2004

Journal of Biological Chemistry

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“…Adherent PECs were pulsed with lysine-fi xable dextran Texas red (0.5 mg/ml, 10 kD; Invitrogen) for 1 h. After washing and 3 h of incubation, dextran was chased into lysosomes before GFP-PTG infection (28).…”

Section: Fluorescent Staining and Microscopymentioning

confidence: 99%

Vacuolar and plasma membrane stripping and autophagic elimination of Toxoplasma gondii in primed effector macrophages

Ling¹,

Shaw²,

Ayala³

et al. 2006

The Journal of Cell Biology

103

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Apicomplexan protozoan pathogens avoid destruction and establish a replicative niche within host cells by forming a nonfusogenic parasitophorous vacuole (PV). Here we present evidence for lysosome-mediated degradation of Toxoplasma gondii after invasion of macrophages activated in vivo. Pathogen elimination was dependent on the interferon inducible-p47 GTPase, IGTP, required PI3K activity, and was preceded by PV membrane indentation, vesiculation, disruption, and, surprisingly, stripping of the parasite plasma membrane. Denuded parasites were enveloped in autophagosome-like vacuoles, which ultimately fused with lysosomes. These observations outline a series of mechanisms used by effector cells to redirect the fate of a classically nonfusogenic intracellular pathogen toward a path of immune elimination. CORRESPONDENCE George S. Yap: George_Yap@brown.eduThe online version of this article contains supplemental material.

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A Process for Controlling Intracellular Bacterial Infections Induced by Membrane Injury

Cited by 131 publications

References 22 publications

A Role for Synaptotagmin VII-Regulated Exocytosis of Lysosomes in Neurite Outgrowth from Primary Sympathetic Neurons

A Role for Synaptotagmin VII-Regulated Exocytosis of Lysosomes in Neurite Outgrowth from Primary Sympathetic Neurons

Synaptotagmin VII Is Targeted to Dense-core Vesicles and Regulates Their Ca2+-dependent Exocytosis in PC12 Cells

Vacuolar and plasma membrane stripping and autophagic elimination of Toxoplasma gondii in primed effector macrophages

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