Annotated protein:Neurobeachin (Neurobeachin a). Gene symbol: IM:7138260. Taxonomy: Danio rerio (Zebrafish). Uniprot ID: E7EZD1
antibody wiki:
SynGO gene info:SynGO data @ NBEA
Ontology domain:Biological Process
SynGO term:synapse organization (GO:0050808)
Annotated paper:Miller AC, et al. "Neurobeachin is required postsynaptically for electrical and chemical synapse formation" Curr Biol. 2015 Jan 5;25(1):16-28 PMID:25484298
Figure(s):Fig.3, 4, 6
Annotation description:Fig.3: "Glycinergic synapses are disrupted in nbea mutants"

Fig.4: "Electrical and chemical synaptic scaffolds are disrupted in nbea mutants"

Fig.6: "Neurobeachin is necessary and sufficient in the postsynaptic neuron for electrical and chemical synapse formation"
- "We found that Nbea was also sufficient in the postsynaptic neuron (be it CoLo or M), but not in the presynaptic neuron, to rescue GlyR localization"
- "Taken together we conclude that Nbea is both necessary and sufficient within the postsynaptic neuron for electrical and chemical synapse formation."

- synapse organization
Evidence tracking, Biological System:Intact tissue
Evidence tracking, Protein Targeting:Genetic transformation (eg; knockout, knockin, mutations)
Evidence tracking, Experiment Assay:Confocal
Annotator(s):Pim van Nierop (ORCID:0000-0003-0593-3443)
Guus Smit (ORCID:0000-0002-2286-1587)
Matthijs Verhage (ORCID:0000-0002-2514-0216)
Lab:Department of Functional Genomics, Department of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands
Additional literature:See also:
A challenge in neuroscience is to understand the mechanisms underlying synapse formation. Most excitatory synapses in the brain are built on spines, which are actin-rich protrusions from dendrites. Spines are a major substrate of brain plasticity, and spine pathologies are observed in various mental illnesses. Here we investigate the role of neurobeachin (Nbea), a multidomain protein previously linked to cases of autism, in synaptogenesis. We show that deletion of Nbea leads to reduced numbers of spinous synapses in cultured neurons from complete knockouts and in cortical tissue from heterozygous mice, accompanied by altered miniature postsynaptic currents. In addition, excitatory synapses terminate mostly at dendritic shafts instead of spine heads in Nbea mutants, and actin becomes less enriched synaptically. As actin and synaptopodin, a spine-associated protein with actin-bundling activity, accumulate ectopically near the Golgi apparatus of mutant neurons, a role emerges for Nbea in trafficking important cargo to pre- and postsynaptic compartments. @ PMID:22109531
SynGO annotation ID:3781
Dataset release (version):20231201
View annotation as GO-CAM model:Gene Ontology