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dc.contributor.authorGobius, Ilan*
dc.contributor.authorMorcom, Laura*
dc.contributor.authorSuárez, Rodrigo*
dc.contributor.authorBunt, Jens*
dc.contributor.authorBukshpun, Polina*
dc.contributor.authorReardon, William*
dc.contributor.authorDobyns, William B*
dc.contributor.authorRubenstein, John L R*
dc.contributor.authorBarkovich, A James*
dc.contributor.authorSherr, Elliott H*
dc.contributor.authorRichards, Linda J*
dc.date.accessioned2018-04-23T12:19:43Z
dc.date.available2018-04-23T12:19:43Z
dc.date.issued2016
dc.identifier.citationAstroglial-Mediated Remodeling of the Interhemispheric Midline Is Required for the Formation of the Corpus Callosum. 2016, 17 (3):735-747 Cell Repen
dc.identifier.issn2211-1247
dc.identifier.pmid27732850
dc.identifier.doi10.1016/j.celrep.2016.09.033
dc.identifier.urihttp://hdl.handle.net/10147/622959
dc.description.abstractThe corpus callosum is the major axon tract that connects and integrates neural activity between the two cerebral hemispheres. Although ∼1:4,000 children are born with developmental absence of the corpus callosum, the primary etiology of this condition remains unknown. Here, we demonstrate that midline crossing of callosal axons is dependent upon the prior remodeling and degradation of the intervening interhemispheric fissure. This remodeling event is initiated by astroglia on either side of the interhemispheric fissure, which intercalate with one another and degrade the intervening leptomeninges. Callosal axons then preferentially extend over these specialized astroglial cells to cross the midline. A key regulatory step in interhemispheric remodeling is the differentiation of these astroglia from radial glia, which is initiated by Fgf8 signaling to downstream Nfi transcription factors. Crucially, our findings from human neuroimaging studies reveal that developmental defects in interhemispheric remodeling are likely to be a primary etiology underlying human callosal agenesis.
dc.language.isoenen
dc.publisherCellPressen
dc.relation.urlhttps://www.sciencedirect.com/science/article/pii/S2211124716312554?via%3Dihuben
dc.rightsArchived with thanks to Cell reportsen
dc.subjectDEVELOPMENTAL DISORDERen
dc.subjectBRAINen
dc.subject.meshAgenesis of Corpus Callosum
dc.subject.meshAnimals
dc.subject.meshAstrocytes
dc.subject.meshAxons
dc.subject.meshCell Differentiation
dc.subject.meshCerebrum
dc.subject.meshCorpus Callosum
dc.subject.meshFibroblast Growth Factor 8
dc.subject.meshHumans
dc.subject.meshMice
dc.subject.meshOrganogenesis
dc.subject.meshPhenotype
dc.subject.meshSignal Transduction
dc.subject.meshTranscription Factors
dc.subject.otherCorpus Callosumen
dc.subject.otherNEUROIMAGINGen
dc.titleAstroglial-Mediated Remodeling of the Interhemispheric Midline Is Required for the Formation of the Corpus Callosum.en
dc.typeArticleen
dc.identifier.journalCell reportsen
dc.description.fundingOtheren
dc.description.provinceLeinsteren
dc.description.peer-reviewpeer-reviewen
refterms.dateFOA2018-09-03T09:28:01Z
html.description.abstractThe corpus callosum is the major axon tract that connects and integrates neural activity between the two cerebral hemispheres. Although ∼1:4,000 children are born with developmental absence of the corpus callosum, the primary etiology of this condition remains unknown. Here, we demonstrate that midline crossing of callosal axons is dependent upon the prior remodeling and degradation of the intervening interhemispheric fissure. This remodeling event is initiated by astroglia on either side of the interhemispheric fissure, which intercalate with one another and degrade the intervening leptomeninges. Callosal axons then preferentially extend over these specialized astroglial cells to cross the midline. A key regulatory step in interhemispheric remodeling is the differentiation of these astroglia from radial glia, which is initiated by Fgf8 signaling to downstream Nfi transcription factors. Crucially, our findings from human neuroimaging studies reveal that developmental defects in interhemispheric remodeling are likely to be a primary etiology underlying human callosal agenesis.


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