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10.7554/eLife.12790.014 Figure 8. Collapse model for vesicle tethering at the TGN.
We propose a new mechanistic model for vesicle exocytosis in auditory hair cells where the rate of vesicle recruitment to the ribbons is directly controlled by a synaptic F-actin network and changes in intracellular hydrostatic pressure.
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We discuss this now more carefully in the text with a reference to this paper (in the subsection headed "Minimal vesicle state model for synaptic vesicle release").
A structural model for a vesicle consistent with this stoichiometry is developed and used in the computation of excitonic properties.
The mechanistic model for autophagic vesicle dynamics presented here reproduced empirical data and proved to be predictive through experimental tests.
We tested LUVs as a membrane model of organelle such as mitochondria as well as SUVs as a membrane model for synaptic vesicles.
I will not discuss this terminology or the data that led to it in detail, as the various arguments have already been presented (Rizzoli & Betz, 2005; Denker & Rizzoli, 2010) (see also Pan & Zucker, 2009 for a quantitative model of vesicle pool activity).
Recently determined structures of the SNARE complex, synaptotagmin III, nSec1, domains of the NSF chaperone and its adaptor (SNAP), and Rab3 and some of its effectors provide the framework for developing molecular models of vesicle fusion and for designing experiments to test these models.
In this paper, a phase field model is developed for vesicle adhesion involving complex substrate and vesicle geometries.
Two major models for synaptic vesicle endocytosis have emerged from studies of ultrastructure: clathrin-mediated endocytosis and kiss-and-run endocytosis.
The AP-1 binding site (939 1,031)is essential for GCC185's role in vesicle tethering but not Golgi ribbon maintenance (Brown, Schindelhaim, and Pfeffer, 2011), and it must be included in any model of vesicle tethering".
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com