ArticleNature communications2024
Semaphorin heterodimerization in cis regulates membrane targeting and neocortical wiring.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Structurally exclusive Teneurin complexes orchestrate divergent programs in early cortical development.Nature communications · 2026Article
- Sequestration of growth cone surface proteins by cytoplasmic Lrrtm2 inducesbioRxiv : the preprint server for biology · 2026Article
- Transcription factor 4 regulates the interhemispheric midline remodeling through neuron-astroglia communications during corpus callosum formation.Translational psychiatry · 2025Article
- Mef2c Controls Postnatal Callosal Axon Targeting by Regulating Sensitivity to Ephrin Repulsion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Generation of human induced pluripotent stem cell lines derived from a patient carrying an intragenic deletion in the NFIA gene.Human cell · 2025Article
- The role of macrophages in vascular calcification: strategies for diagnosis and treatment.Frontiers in immunology · 2025Review
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Authors and funding
16 authors.
Funding
Abstract
Disruption of neocortical circuitry and architecture in humans causes numerous neurodevelopmental disorders. Neocortical cytoarchitecture is orchestrated by various transcription factors such as Satb2 that control target genes during strict time windows. In humans, mutations of SATB2 cause SATB2 Associated Syndrome (SAS), a multisymptomatic syndrome involving epilepsy, intellectual disability, speech delay, and craniofacial defects. Here we show that Satb2 controls neuronal migration and callosal axonal outgrowth during murine neocortical development by inducing the expression of the GPI-anchored protein, Semaphorin 7A (Sema7A). We find that Sema7A exerts this biological activity by heterodimerizing in cis with the transmembrane semaphorin, Sema4D. We could also observe that heterodimerization with Sema7A promotes targeting of Sema4D to the plasma membrane in vitro. Finally, we report an epilepsy-associated de novo mutation in Sema4D (Q497P) that inhibits normal glycosylation and plasma membrane localization of Sema4D-associated complexes. These results suggest that neuronal use of semaphorins during neocortical development is heteromeric, and a greater signaling complexity exists than was previously thought.
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Registered trials
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