ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Genetic evidence for the adhesion protein IgSF9/Dasm1 to regulate inhibitory synapse development independent of its intracellular domain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Targeting immunoglobulin superfamily member 9 (IGSF9) to overcome acute myeloid leukemia resistance to CAR-T therapy.Journal of experimental & clinical cancer research : CR · 2026Article
- Inflammatory mechanisms contribute to long-term cognitive deficits induced by perinatal asphyxia via interleukin-1.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- The role of cell adhesion molecule IgSF9b at the inhibitory synapse and psychiatric disease.Neuroscience and biobehavioral reviews · 2024Review
- Prickle2 and Igsf9b Coordinately Regulate the Cytoarchitecture of the Axon Initial Segment.Cell structure and function · 2020Article
- A Novel Schizophrenia Diagnostic Model Based on Statistically Significant Changes in Gene Methylation in Specific Brain Regions.BioMed research international · 2020Article
- IdentifiedCancer cell international · 2020Article
- The Conserved IgSF9 Protein Borderless Regulates Axonal Transport of Presynaptic Components and Color Vision inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Changes in Deoxyribonucleic Acid Methylation Contribute to the Pathophysiology of Multiple Sclerosis.Frontiers in genetics · 2019Review
- Long‑term treatment with salicylate enables NMDA receptors and impairs AMPA receptors in C57BL/6J mice inner hair cell ribbon synapse.Molecular medicine reports · 2019Article
- IgSF9b regulates anxiety behaviors through effects on centromedial amygdala inhibitory synapses.Nature communications · 2018Article
- TheScience translational medicine · 2018Article
- Immunoglobulin-Like Receptors and Their Impact on Wiring of Brain Synapses.Annual review of genetics · 2018Review
- Unique Sensory and Motor Behavior in Thy1-GFP-M Mice before and after Spinal Cord Injury.Journal of neurotrauma · 2018Article
- Turtle interacts with borderless in regulating glial extension and axon ensheathment.Molecular brain · 2017Article
- Regulation of GABAergic synapse development by postsynaptic membrane proteins.Brain research bulletin · 2017Review
- A dual-strategy expression screen for candidate connectivity labels in the developing thalamus.PloS one · 2017Article
- Homozygous mutation in the APOA1BP is associated with a lethal infantile leukoencephalopathy.Neurogenetics · 2016Article
- Article
- Deciphering H3K4me3 broad domains associated with gene-regulatory networks and conserved epigenomic landscapes in the human brain.Translational psychiatry · 2015Article
- MRCKβ links Dasm1 to actin rearrangements to promote dendrite development.The Journal of biological chemistryArticle
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Normal brain function requires balanced development of excitatory and inhibitory synapses. An imbalance in synaptic transmission underlies many brain disorders such as epilepsy, schizophrenia, and autism. Compared with excitatory synapses, relatively little is known about the molecular control of inhibitory synapse development. We used a genetic approach in mice to identify the Ig superfamily member IgSF9/Dasm1 as a candidate homophilic synaptic adhesion protein that regulates inhibitory synapse development. IgSF9 is expressed in pyramidal cells and subsets of interneurons in the CA1 region of hippocampus. Electrophysiological recordings of acute hippocampal slices revealed that genetic inactivation of the IgSF9 gene resulted in fewer functional inhibitory synapses; however, the strength of the remaining synapses was unaltered. These physiological abnormalities were correlated with decreased expression of inhibitory synapse markers in IgSF9(-/-) mice, providing anatomical evidence for a reduction in inhibitory synapse numbers, whereas excitatory synapse development was normal. Surprisingly, knock-in mice expressing a mutant isoform of IgSF9 lacking the entire cytoplasmic domain (IgSF9(ΔC/ΔC) mice) had no defects in inhibitory synapse development, providing genetic evidence that IgSF9 regulates synapse development via ectodomain interactions rather than acting itself as a signaling receptor. Further, we found that IgSF9 mediated homotypic binding and cell aggregation, but failed to induce synapse formation, suggesting that IgSF9 acts as a cell adhesion molecule (CAM) to maintain synapses. Juvenile IgSF9(-/-) mice exhibited increased seizure susceptibility indicative of an imbalance in synaptic excitation and inhibition. These results provide genetic evidence for a specific role of IgSF9 in inhibitory synapse development/maintenance, presumably by its CAM-like activity.
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