ArticlePloS one2011
Mutation of Semaphorin-6A disrupts limbic and cortical connectivity and models neurodevelopmental psychopathology.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Neurodevelopmental Phenotypes and Brain Anomalies in Individuals With Heterozygous SEMA6A Variants.Clinical genetics · 2026Article
- MidbrainbioRxiv : the preprint server for biology · 2026Article
- Diverse and location-specific roles of PlexinA2, PlexinA4, and NCAM in developing hippocampal mossy fibers.Translational psychiatry · 2026Article
- Transcriptome Analyses Revealed the Genetic Advantages in Polygynous Males ofEcology and evolution · 2025Article
- Transcriptome Study in Sicilian Patients with Autism Spectrum Disorder.Biomedicines · 2024Article
- Variability in Neural Circuit Formation.Cold Spring Harbor perspectives in biology · 2024Review
- Molecular signature of extracellular matrix pathology in schizophrenia.The European journal of neuroscience · 2021Article
- Neuroimaging genetic associations betweenJournal of clinical and experimental neuropsychology · 2021Article
- Semaphorin 6A-Plexin A2/A4 Interactions with Radial Glia Regulate Migration Termination of Superficial Layer Cortical Neurons.iScience · 2019Article
- Semaphorin 6A Attenuates the Migration Capability of Lung Cancer Cells via the NRF2/HMOX1 Axis.Scientific reports · 2019Article
- In vivo epigenetic editing of Sema6a promoter reverses transcallosal dysconnectivity caused by C11orf46/Arl14ep risk gene.Nature communications · 2019Article
- Data for 3D reconstruction of the corticospinal tract in the wild-type and Semaphorin 6A knockout adult brain.Data in brief · 2019Article
- The extracellular SEMA domain attenuates intracellular apoptotic signaling of semaphorin 6A in lung cancer cells.Oncogenesis · 2018Article
- PlexinA2 Forward Signaling through Rap1 GTPases Regulates Dentate Gyrus Development and Schizophrenia-like Behaviors.Cell reports · 2018Article
- Semaphorin-Plexin signaling influences early ventral telencephalic development and thalamocortical axon guidance.Neural development · 2017Article
- A novel relationship for schizophrenia, bipolar and major depressive disorder Part 5: a hint from chromosome 5 high density association screen.American journal of translational research · 2017Article
- Semaphorins and their Signaling Mechanisms.Methods in molecular biology (Clifton, N.J.) · 2017Review
- Transmembrane semaphorins: Multimodal signaling cues in development and cancer.Cell adhesion & migration · 2016Review
- Comprehensive behavioral phenotyping of a new Semaphorin 3 F mutant mouse.Molecular brain · 2016Article
- Reverse Signaling by Semaphorin-6A Regulates Cellular Aggregation and Neuronal Morphology.PloS one · 2016Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psychiatric disorders such as schizophrenia and autism are characterised by cellular disorganisation and dysconnectivity across the brain and can be caused by mutations in genes that control neurodevelopmental processes. To examine how neurodevelopmental defects can affect brain function and behaviour, we have comprehensively investigated the consequences of mutation of one such gene, Semaphorin-6A, on cellular organisation, axonal projection patterns, behaviour and physiology in mice. These analyses reveal a spectrum of widespread but subtle anatomical defects in Sema6A mutants, notably in limbic and cortical cellular organisation, lamination and connectivity. These mutants display concomitant alterations in the electroencephalogram and hyper-exploratory behaviour, which are characteristic of models of psychosis and reversible by the antipsychotic clozapine. They also show altered social interaction and deficits in object recognition and working memory. Mice with mutations in Sema6A or the interacting genes may thus represent a highly informative model for how neurodevelopmental defects can lead to anatomical dysconnectivity, resulting, either directly or through reactive mechanisms, in dysfunction at the level of neuronal networks with associated behavioural phenotypes of relevance to psychiatric disorders. The biological data presented here also make these genes plausible candidates to explain human linkage findings for schizophrenia and autism.
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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.