ArticleNature communications2021
Canonical versus non-canonical transsynaptic signaling of neuroligin 3 tunes development of sociality in mice.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- Synaptic Ca2+ channels and neurexins are linked through direct and indirect binding complexes.Scientific reports · 2026Article
- Transcriptome profiling of neurexin- and neuroligin-deficient Caenorhabditis elegans reveals pathways underlying developmental and behavioral dysfunction.Research square · 2026Article
- A noncanonical neuroligin 3-centered complex promotes functional recovery of spinal cord injury.Stem cell research & therapy · 2026Article
- FOXG1 Hierarchically Shapes Synaptic Functions in Striatal iSPNs and Contributes to ASD Etiology.Neuroscience bulletin · 2026Article
- Alternative microexon splicing code for a four-amino acid peptide of PTPRD governs behavioral development.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Synaptic Cell Adhesion: A Structural Perspective.Advances in neurobiology · 2026Review
- Synaptic and Non-Synaptic Functions of PTPRD: A Receptor Tyrosine Phosphatase at the Crossroads of Neural Circuitry and Metabolism.Journal of neurochemistry · 2025Review
- Training Schedule Affects Operant Responding Independent of Motivation in the Neuroligin-3 R451C Mouse Model of Autism.Genes, brain, and behavior · 2025Article
- A UFD1 variant encoding a microprotein modulates UFD1f and IPMK ubiquitination to play pivotal roles in anti-stress responses.Nature communications · 2025Article
- Alternatively spliced mini-exon B in PTPδ regulates excitatory synapses through cell-type-specific trans-synaptic PTPδ-IL1RAP interaction.Nature communications · 2025Article
- Astrocytic Neuroligin-3 influences gene expression and social behavior, but is dispensable for synapse number.Molecular psychiatry · 2025Article
- Transcriptomic Changes and Pathological Mechanisms in Familial and Sporadic Idiopathic Restless Legs Syndrome: Implications for Inflammation and Cell Adhesion Molecules.Nature and science of sleep · 2025Article
- Sex differences in morphine sensitivity of neuroligin-3 knockout mice.Psychopharmacology · 2024Article
- Neural Influences on Tumor Progression Within the Central Nervous System.CNS neuroscience & therapeutics · 2024Review
- Effects of Human Neural Stem Cells Overexpressing Neuroligin and Neurexin in a Spinal Cord Injury Model.International journal of molecular sciences · 2024Article
- Loss of protein tyrosine phosphatase receptor delta PTPRD increases the number of cortical neurons, impairs synaptic function and induces autistic-like behaviors in adult mice.Biological research · 2024Article
- Differential contribution of canonical and noncanonical NLGN3 pathways to early social development and memory performance.Molecular brain · 2024Article
- Unraveling the Role of Neuroligin3 in Autism Spectrum Disorders: Pathophysiological Insights and Targeted Therapies.CNS & neurological disorders drug targets · 2024Review
Corrections and comments
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Authors and funding
26 authors at 12 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroligin 3 (NLGN3) and neurexins (NRXNs) constitute a canonical transsynaptic cell-adhesion pair, which has been implicated in autism. In autism spectrum disorder (ASD) development of sociality can be impaired. However, the molecular mechanism underlying NLGN3-mediated social development is unclear. Here, we identify non-canonical interactions between NLGN3 and protein tyrosine phosphatase δ (PTPδ) splice variants, competing with NRXN binding. NLGN3-PTPδ complex structure revealed a splicing-dependent interaction mode and competition mechanism between PTPδ and NRXNs. Mice carrying a NLGN3 mutation that selectively impairs NLGN3-NRXN interaction show increased sociability, whereas mice where the NLGN3-PTPδ interaction is impaired exhibit impaired social behavior and enhanced motor learning, with imbalance in excitatory/inhibitory synaptic protein expressions, as reported in the Nlgn3 R451C autism model. At neuronal level, the autism-related Nlgn3 R451C mutation causes selective impairment in the non-canonical pathway. Our findings suggest that canonical and non-canonical NLGN3 pathways compete and regulate the development of sociality.
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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.