Semaphorin 6A–Plexin A2/A4 Interactions with Radial Glia Regulate Migration Termination of Superficial Layer Cortical Neurons

Precise regulation of neuronal migration termination is crucial for the establishment of brain cytoarchitectures. However, little is known about how neurons terminate migration. Here we focused on interactions between migrating cortical neurons and their substrates, radial glial (RG) cells, and anal...

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Published iniScience Vol. 21; pp. 359 - 374
Main Authors Hatanaka, Yumiko, Kawasaki, Takahiko, Abe, Takaya, Shioi, Go, Kohno, Takao, Hattori, Mitsuharu, Sakakibara, Akira, Kawaguchi, Yasuo, Hirata, Tatsumi
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 22.11.2019
Elsevier
Subjects
Biological Sciences
Cellular Neuroscience
Molecular Biology
Molecular Neuroscience
Neuroscience
Biological Sciences
Neuroscience
Cellular Neuroscience
Molecular Biology
Molecular Neuroscience
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Summary:Precise regulation of neuronal migration termination is crucial for the establishment of brain cytoarchitectures. However, little is known about how neurons terminate migration. Here we focused on interactions between migrating cortical neurons and their substrates, radial glial (RG) cells, and analyzed the role of Plexin A2 and A4 (PlxnA2/A4) receptors and their repulsive ligand, Semaphorin 6A (Sema6A), for this process. In both PlxnA2/A4 double-knockout and Sema6A mutant mice, the outermost cortical plate neurons ectopically invade layer 1 at a stage when they should reach their destinations. PlxnA2/A4 proteins are abundantly expressed on their leading processes, whereas Sema6A mRNA is enriched in RG cell somata. Cell-targeted gene expression and conditional knockouts indicate critical roles for these molecules. We hypothesize that the timely appearance of repulsive signaling mediated by Sema6A–PlxnA2/A4 weakens migrating neuron–RG cell interactions, leading to migration termination. [Display omitted] •Loss of PlxnA2/A4 results in superficial layer neurons invading layer 1•PlxnA2/A4 works cell autonomously to settle these neurons properly•Lack of Sema6A in radial glial cells causes similar mispositioning of these neurons•Sema6A–PlxnA2/A4 signaling determines settling position of superficial layer neurons Biological Sciences; Molecular Biology; Neuroscience; Molecular Neuroscience; Cellular Neuroscience
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These authors contributed equally to the experimental part of this study
ISSN:2589-0042
2589-0042
DOI:10.1016/j.isci.2019.10.034