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Rab Cascades

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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.

Autophagy

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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Recycling Endosomes and Transcytosis

The recycling endosome, also known as the endosomal recycling compartment (ERC), is a part of the slow-recycling process of the endocytic pathway. Molecules internalized through receptor-mediated endocytosis are either degraded in the lysosomes or are recycled to the plasma membrane through the fast- or slow-recycling route.
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Delivery Pathways to the Lysosome

Delivery Pathways to the Lysosome

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Endocytosis
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Rab Proteins

Rab Proteins

Rab proteins constitute the largest family of monomeric GTPases, of which 70 members are present in humans. Rab proteins and their effectors regulate consecutive stages of vesicle transport such as vesicle transport, docking, and fusion to the correct recipient membrane.
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Pinching-off of Coated Vesicles

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Related Experiment Video

Updated: May 23, 2025

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins

Published on: June 26, 2018

Autophagy at the postsynapse begins with Rab11 and does not end with dendritic spine pruning.

Aleksandra Janusz-Kaminska¹, Jacek Jaworski²

¹Department of Cell Biology, Emory University School of Medicine, Atlanta, GA, USA.

Autophagy Reports

|May 21, 2025

Summary

Rab11 protein initiates autophagy in dendritic spines by maintaining Atg9A, enabling vesicle formation at the postsynapse. This process, linked to NMDA receptor stimulation, does not appear to cause dendritic spine pruning.

Keywords:

Atg9A Rab11 autophagy dendritic spines mTOR neurons synaptic plasticity

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Last Updated: May 23, 2025

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins

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Published on: June 26, 2018

3D Modeling of Dendritic Spines with Synaptic Plasticity

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Published on: May 18, 2020

Purification of the Dendritic Filopodia-rich Fraction

Purification of the Dendritic Filopodia-rich Fraction

Published on: May 2, 2019

Area of Science:

Neuroscience
Cell Biology
Molecular Biology

Background:

Neurons exhibit localized autophagy crucial for synaptic plasticity.
The initial steps and postsynaptic roles of autophagy remain largely uncharacterized.

Purpose of the Study:

To investigate the role of Rab11 in initiating autophagy within dendritic spines.
To elucidate the function of autophagic compartments at the postsynaptic site.

Main Methods:

Focuses on Rab11's role in dendritic spine autophagy.
Examines the maintenance of Atg9A by Rab11.
Investigates the emergence of LC3+ vesicles at the postsynapse.

Main Results:

Rab11 was found to maintain Atg9A within dendritic spines.
Rab11 is essential for the formation of LC3-positive vesicles at the postsynapse.
Autophagosome formation is hypothesized to involve NMDA receptor stimulation and local mTOR activity.

Conclusions:

Rab11 plays a critical role in the initiation of autophagy in dendritic spines.
Autophagosomes may not be responsible for dendritic spine pruning, contrary to some hypotheses.