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Related Concept Videos

Fusion of Secretory Vesicles with the Plasma Membrane01:26

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Proteins and neurotransmitters in secretory vesicles can be released from a cell upon vesicle docking, priming, and fusion with the plasma membrane. Vesicles are docked and primed in preparation for the quick exocytosis of their contents in response to a stimulus. The fusion process is mainly carried out by a SNAP Receptor or SNARE complex, consisting of synaptobrevin, syntaxin-1, and SNAP-25.
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Vesicle budding is orchestrated by distinct cytosolic proteins such as adaptor proteins, coat proteins, and GTPases. To initiate vesicle budding, membrane-bending proteins containing crescent-shaped BAR domains bind to the lipid heads in the bilayer and distort the membrane to form a protein-coated vesicle bud. Adaptors proteins such as AP2 for clathrin-coated vesicles can nucleate on the deformed membrane. Finally, coat proteins such as clathrin or COPI and COPII assemble into a coat forming...
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Rab GTPases act in a regulated cascade during membrane fusion, helping the lipid bilayers mix. The Rab family of proteins are active when bound to GTP, and inactive when bound to GDP. Hence, they act as guanine nucleotide-dependent molecular switches. Rab-GTP recognizes and binds to long or short-range tethering proteins to capture the target vesicle. These tethers coordinate with SNAREs on the vesicle and the target membrane to assemble the trans SNARE complex that locks the mixing bilayers.
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Once a transport vesicle has recognized its target organelle, the vesicular membrane needs to fuse with the target membrane to unload the cargo. Transmembrane proteins called SNAREs present on organelle membranes and their vesicles, mediate vesicle fusion.
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Neurons: The Axon01:21

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Axons are long, cytoplasmic processes of nerve cells capable of propagating electrical impulses known as action potentials. The cytoplasm or axoplasm of an axon contains neurofibrils, neurotubules, small vesicles, lysosomes, mitochondria, and various enzymes, all encased within the axolemma, the plasma membrane of the axon.
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Related Experiment Video

Updated: Jun 23, 2025

Utilizing Combined Methodologies to Define the Role of Plasma Membrane Delivery During Axon Branching and Neuronal Morphogenesis
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An initial HOPS-mediated fusion event is critical for autophagosome transport initiation from the axon terminal.

Serena R Wisner1,2, Madison Chlebowski1, Amrita Mandal3

  • 1Department of Integrative Biology, University of Wisconsin-Madison, Madison, WI, USA.

Autophagy
|June 20, 2024
PubMed
Summary

The HOPS complex is crucial for neuronal autophagy, enabling autophagosome maturation and retrograde transport initiation from axon terminals. This finding clarifies the cellular pathology of HOPS-complex linked neurodegenerative diseases.

Keywords:
Axon terminalVps18autophagyaxonal transportlysosomeneuron

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Neuronal autophagy is vital for cell health, involving autophagosome formation in axon terminals and retrograde transport for maturation and degradation.
  • Disrupting neuronal autophagy or autophagosome transport negatively impacts neuronal function.
  • The molecular mechanisms initiating retrograde autophagosome transport from axon terminals remain incompletely understood.

Purpose of the Study:

  • To investigate the role of the HOPS (homotypic fusion and protein sorting) complex in neuronal autophagy and autophagosome transport.
  • To determine if HOPS complex function is essential for autophagosome maturation and retrograde transport initiation in neurons.

Main Methods:

  • Utilized zebrafish strains with loss-of-function mutations in HOPS complex components (vps18 and vps41).
  • Confirmed HOPS complex disruption by analyzing endogenous deletion of the HOPS binding domain in Vps18.
  • Employed pharmacological inhibition of lysosomal proteases to assess the requirement of autophagosome maturation for transport initiation.

Main Results:

  • Disruption of the HOPS complex in zebrafish eliminated autophagosome maturation.
  • Loss of HOPS function specifically disrupted the initiation of retrograde autophagosome transport from axon terminals.
  • Pharmacological inhibition demonstrated that autophagosome maturation is a prerequisite for initiating retrograde transport.

Conclusions:

  • HOPS-mediated fusion events are critical for promoting autophagosome maturation.
  • HOPS complex function is essential for initiating retrograde autophagosome transport from neuronal axon terminals.
  • This study reveals key roles for the HOPS complex in neuronal autophagy and provides insights into HOPS-complex linked neurodegenerative diseases.