ArticlePloS one2015
Mutational Analysis of Rab3 Function for Controlling Active Zone Protein Composition at the Drosophila Neuromuscular Junction.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- An ArfGAP-dependent signaling modulates synaptic plasticity via IP3-regulated calcium release from the endoplasmic reticulum.PLoS genetics · 2026Article
- Heterozygous RAB3A variants cause cerebellar ataxia by a partial loss-of-function mechanism.Brain : a journal of neurology · 2025Article
- Blobby is a synaptic active zone assembly protein required for memory in Drosophila.Nature communications · 2025Article
- Presynaptic regulators in memory formation.Learning & memory (Cold Spring Harbor, N.Y.) · 2024Article
- Versatile CRISPR/Cas9-mediated mosaic analysis by gRNA-induced crossing-over for unmodified genomes.PLoS biology · 2021Article
- Mechanisms of α-Synuclein Induced Synaptopathy in Parkinson's Disease.Frontiers in neuroscience · 2018Review
- Presynaptic morphogenesis, active zone organization and structural plasticity in Drosophila.Current opinion in neurobiology · 2017Review
- The Drosophila KIF1A Homolog unc-104 Is Important for Site-Specific Synapse Maturation.Frontiers in cellular neuroscience · 2016Article
- Synaptic Vesicle Proteins and Active Zone Plasticity.Frontiers in synaptic neuroscience · 2016Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
At synapses, the release of neurotransmitter is regulated by molecular machinery that aggregates at specialized presynaptic release sites termed active zones. The complement of active zone proteins at each site is a determinant of release efficacy and can be remodeled to alter synapse function. The small GTPase Rab3 was previously identified as playing a novel role that controls the distribution of active zone proteins to individual release sites at the Drosophila neuromuscular junction. Rab3 has been extensively studied for its role in the synaptic vesicle cycle; however, the mechanism by which Rab3 controls active zone development remains unknown. To explore this mechanism, we conducted a mutational analysis to determine the molecular and structural requirements of Rab3 function at Drosophila synapses. We find that GTP-binding is required for Rab3 to traffick to synapses and distribute active zone components across release sites. Conversely, the hydrolytic activity of Rab3 is unnecessary for this function. Through a structure-function analysis we identify specific residues within the effector-binding switch regions that are required for Rab3 function and determine that membrane attachment is essential. Our findings suggest that Rab3 controls the distribution of active zone components via a vesicle docking mechanism that is consistent with standard Rab protein function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.