Axolemmal repair requires proteins that mediate synaptic vesicle fusion

Detrait, Eric; Eddleman, Christopher S.; Yoo, Soonmoon; Fukuda, Mitsunori; Nguyen, Michael P.; Bittner, George D.; Fishman, Harvey M.

doi:10.1002/1097-4695(20000915)44:4<382::aid-neu2>3.0.co;2-q

Cited by 53 publications

(45 citation statements)

References 42 publications

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“…Botulinum or tetanus toxins, injected into fibroblasts or sea urchin eggs, inhibit resealing, suggesting a requirement for SNAREs (Steinhardt et al, 1994). Injection of functionneutralizing antibodies or competitive peptide fragments of synaptotagmin VII into fibroblasts (Reddy et al, 2001) or squid giant axons (Detrait et al, 2000a;Detrait et al, 2000b) partially inhibit resealing, suggesting a role for this possible Ca 2+ sensor. However, a recent study casts doubt on the role of synaptotagmin VII (Jaiswal et al, 2004): it showed that, in fibroblasts at least, synaptotagmin VII actually acts as a brake on the resealing-based exocytotic event it was supposed to mediate.…”

Section: Introductionmentioning

confidence: 99%

Yolk granule tethering: a role in cell resealing and identification of several protein components

McNeil

2005

Journal of Cell Science

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Homotypic fusion among echinoderm egg yolk granules has previously been reconstituted in vitro, and shown to be a rapid, Ca2+-triggered reaction that can produce extremely large (>10 μm diameter) fusion products. We here show that, prior to Ca2+-triggered fusion, yolk granules in vitro, if isolated in an appropriate buffer, became tethered to one another, forming large aggregates of more than 100 granules. Granule washing with mildly chaotropic salt abolished this tethering reaction, and prevented Ca2+-triggered formation of the large fusion products characteristic of tethered granules. Protein factors present in the wash restored tethering activity and these factors could be substantially enriched by anion exchange chromatography. The enriched fraction behaved under native conditions as a high molecular weight (∼670 kDa), multisubunit complex of at least seven proteins. Monoclonal antibodies directed against this complex of proteins were capable of immunodepleting tethering activity, confirming the role of the complex in granule tethering. These antibodies selectively stained the surface of yolk granules in the intact egg. We therefore propose a new role for tethering: it can promote the formation of large vesicular fusion products, such as those required for successful resealing. We have, moreover, identified several proteins that may be critical to this tethering mechanism.

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Section: Introductionmentioning

confidence: 99%

Yolk granule tethering: a role in cell resealing and identification of several protein components

McNeil

2005

Journal of Cell Science

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“…Syts III, IV, VI, and VII) are localized at membranes other than classical secretory vesicles and regulate distinct types of Ca 2ϩ -dependent exocytosis (e.g. lysosomal exocytosis, plasma membrane repair, and acrosomal reaction) (23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33).…”

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confidence: 99%

Synaptotagmin V Is Targeted to Dense-core Vesicles That Undergo Calcium-dependent Exocytosis in PC12 Cells

Saegusa¹,

Fukuda²,

Mikoshiba³

2002

Journal of Biological Chemistry

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Chem. 274, 31421-31427). Although they have been suggested to be involved in vesicular trafficking, as in the role of the Syt I isoform in synaptic vesicle exocytosis, their exact functions remain to be clarified, and even their precise subcellular localization is still a matter of controversy. In this study, we established rat pheochromocytoma (PC12) cell lines that stably express Syts III-, V-, VI-, and X-GFP (green fluorescence protein) fusion proteins, respectively, to determine their precise subcellular localizations. Surprisingly, Syts III-, V-, VI-, and X-GFP proteins were found to be targeted to specific organelles: Syt III-GFP to near the plasma membrane, Syt V-GFP to dense-core vesicles, Syt VI-GFP to endoplasmic reticulum-like structures, and Syt X-GFP to vesicles (other than dense-core vesicles) present in cytoplasm. We showed that Syt V-containing vesicles at the neurites of PC12 cells were processed to exocytosis in a Ca 2؉ -dependent manner. Immunohistochemical analysis further showed that endogenous Syt V was also localized on dense-core vesicles in the mouse brain and specifically expressed in glucagon-positive ␣-cells in mouse pancreatic islets, but not in ␤-or ␦-cells. Based on these results, we propose that Syt V is a dense-core vesicle-specific Syt isoform that controls a specific type of Ca 2؉ -regulated secretion.

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“…Interestingly, neurotransmission inhibitors botulinum neurotoxin " and " also negatively afected or completely blocked membrane healing in sea urchin embryos and Swiss 3T3 ibroblasts [ 8]. Similarly, treatment with an antibody targeting the active synaptotagmin I C " domain was observed to prevent membrane resealing of squid and crayish giant axons [ 08], 3T3 ibroblasts [ 00] and rat PC cells [ 0 ]. In contrast to the neuron-speciic synaptotagmin I [ 0], synaptotagmin VII is ubiquitously expressed and has been found to also inluence exocytic membrane repair of other cell types such as sea urchin embryos [ 8,03] ].…”

Section: Neuronal Cells and Ibroblasts: Insights Into Exocytic mentioning

confidence: 99%

How Plasma Membrane and Cytoskeletal Dynamics Influence Single-Cell Wound Healing: Mechanotransduction, Tension and Tensegrity

Boucher¹,

Kato²,

Mandato³

2016

Wound Healing - New Insights Into Ancient Challenges

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Organisms are able to recover from injuries by replacing damaged tissues, which recover by replacing damaged cells and extracellular structures. Similarly, a cell recovers from injuries by replacing damaged components of its structural integrity its plasma membrane and cytoskeletal structures. Cells can be thought of as tensegral structures, their structural integrity relying on the interplay between tensile forces generated within and without the cell, and the compressive elements that counteracts them. "s such, direct or indirect insults to the plasma membrane or cytoskeleton of a cell may not only result in the temporary loss of structural integrity, but also directly impact its ability to respond to its environment. This chapter will focus on the various aspects linking tensile forces and single-cell wound healing where and how are they generated, how does the cell counteract them and how does the cell return to its previous tensegrity state? These questions will be explored using ubiquitous and cell-type speciic examples of singlecell repair processes. Special atention will be given to changes in plasma membrane composition and area to cytoskeletal dynamics, and how these factor each other to inluence and efect single-cell repair.

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Axolemmal repair requires proteins that mediate synaptic vesicle fusion

Cited by 53 publications

References 42 publications

Yolk granule tethering: a role in cell resealing and identification of several protein components

Yolk granule tethering: a role in cell resealing and identification of several protein components

Synaptotagmin V Is Targeted to Dense-core Vesicles That Undergo Calcium-dependent Exocytosis in PC12 Cells

How Plasma Membrane and Cytoskeletal Dynamics Influence Single-Cell Wound Healing: Mechanotransduction, Tension and Tensegrity

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