Annotated protein: | Neurexin-2 (Neurexin II-alpha) (Neurexin-2-alpha). Gene symbol: NRXN2. Taxonomy: Mus musculus (Mouse). Uniprot ID: E9Q7X7 |
antibody wiki: | |
SynGO gene info: | SynGO data @ NRXN2 |
Ontology domain: | Biological Process |
SynGO term: | regulation of postsynapse assembly (GO:0150052) |
Synapse type(s): | hippocampus |
Annotated paper: | Lin PY, et al. "Neurexin-2: An inhibitory neurexin that restricts excitatory synapse formation in the hippocampus" Sci Adv. 2023 Jan 6;9(1):eadd8856 PMID:36608123 |
Figure(s): | Figure 1, 4, 5 |
Annotation description: | Figure 1: Constitutive deletion of Nrxn2 increases CA3→CA1 synaptic connections in the hippocampus. Figure 4: STORM superresolution microscopy reveals that the pan-neuronal Nrxn2 deletion (Nrxn2 nKO) increases the excitatory synapse density in the CA1 region. Figure 5: Conditional deletion of Nrxn2 from the hippocampus of adolescent mice enhances the strength of CA3→CA1 synaptic connections "dSTORM imaging of hippocampal sections that were double-labeled for the presynaptic marker Bassoon and the postsynaptic marker Homer1 revealed that, as expected, Bassoon and Homer1 were localized adjacent to each other in large "macroclusters". Notably, the density of Bassoon and Homer1 macroclusters was greatly elevated (>100% increase) in Nrxn2 nKO mice (Fig. 4, D and E)." "In analyzing the dSTORM data, we also noted that the Nrxn2 nKO enlarged the size of Homer1 but not of Bassoon clusters, as revealed by an increase (~75%) in cluster volume, cluster size, particle numbers per cluster, and particle density per cluster (Fig. 4, F and G). This finding suggests that the Nrxn2 nKO enhances the size of postsynaptic but not presynaptic specializations in addition to elevating the synapse density." Authors summarized these data as: "Here we show that Nrxn2, different from Nrxn1 and Nrxn3, functions to restrict, instead of enabling, synapse assembly in the hippocampus. This finding was confirmed by electrophysiological analyses of three different genetic Nrxn2 manipulations, constitutive global deletions (Fig. 1), neuron-specific deletions (Fig. 3), and conditional deletions in which Nrxn2 was selectively ablated postdevelopmentally (Fig. 5). The presence of an increase in synaptic connections induced by the Nrxn2 deletion was established using dSTORM superresolution microscopy (Fig. 4)." |
Evidence tracking, Biological System: | Intact tissue |
Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) |
Evidence tracking, Experiment Assay: | Super resolution Electrophysiology (generic) |
Annotator(s): | Frank Koopmans (ORCID:0000-0002-4973-5732) 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 |
SynGO annotation ID: | 5004 |
Dataset release (version): | 20231201 |
View annotation as GO-CAM model: |