001     155882
005     20240329115604.0
024 7 _ |a 10.3389/fnmol.2021.687581
|2 doi
024 7 _ |a pmid:34220450
|2 pmid
024 7 _ |a pmc:PMC8243374
|2 pmc
024 7 _ |a altmetric:108724043
|2 altmetric
037 _ _ |a DZNE-2021-01042
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Sokpor, Godwin
|b 0
245 _ _ |a Loss of BAF Complex in Developing Cortex Perturbs Radial Neuronal Migration in a WNT Signaling-Dependent Manner.
260 _ _ |a Lausanne
|c 2021
|b Frontiers Research Foundation
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1711633439_27785
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Radial neuronal migration is a key neurodevelopmental event indispensable for proper cortical laminar organization. Cortical neurons mainly use glial fiber guides, cell adhesion dynamics, and cytoskeletal remodeling, among other discrete processes, to radially trek from their birthplace to final layer positions. Dysregulated radial migration can engender cortical mis-lamination, leading to neurodevelopmental disorders. Epigenetic factors, including chromatin remodelers have emerged as formidable regulators of corticogenesis. Notably, the chromatin remodeler BAF complex has been shown to regulate several aspects of cortical histogenesis. Nonetheless, our understanding of how BAF complex regulates neuronal migration is limited. Here, we report that BAF complex is required for neuron migration during cortical development. Ablation of BAF complex in the developing mouse cortex caused alteration in the cortical gene expression program, leading to loss of radial migration-related factors critical for proper cortical layer formation. Of note, BAF complex inactivation in cortex caused defective neuronal polarization resulting in diminished multipolar-to-bipolar transition and eventual disruption of radial migration of cortical neurons. The abnormal radial migration and cortical mis-lamination can be partly rescued by downregulating WNT signaling hyperactivity in the BAF complex mutant cortex. By implication, the BAF complex modulates WNT signaling to establish the gene expression program required for glial fiber-dependent neuronal migration, and cortical lamination. Overall, BAF complex has been identified to be crucial for cortical morphogenesis through instructing multiple aspects of radial neuronal migration in a WNT signaling-dependent manner.
536 _ _ |a 352 - Disease Mechanisms (POF4-352)
|0 G:(DE-HGF)POF4-352
|c POF4-352
|f POF IV
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a BAF complex
|2 Other
650 _ 7 |a Wnt signaling
|2 Other
650 _ 7 |a cell adhesion
|2 Other
650 _ 7 |a cortical development
|2 Other
650 _ 7 |a cortical lamination
|2 Other
650 _ 7 |a glial fibers
|2 Other
650 _ 7 |a neuronal migration
|2 Other
700 1 _ |a Kerimoglu, Cemil
|0 P:(DE-2719)2812366
|b 1
|u dzne
700 1 _ |a Nguyen, Huong
|b 2
700 1 _ |a Pham, Linh
|b 3
700 1 _ |a Rosenbusch, Joachim
|b 4
700 1 _ |a Wagener, Robin
|b 5
700 1 _ |a Nguyen, Huu Phuc
|b 6
700 1 _ |a Fischer, Andre
|0 P:(DE-2719)2000047
|b 7
|u dzne
700 1 _ |a Staiger, Jochen F
|b 8
700 1 _ |a Tuoc, Tran
|b 9
773 _ _ |a 10.3389/fnmol.2021.687581
|g Vol. 14, p. 687581
|0 PERI:(DE-600)2452967-9
|p 687581
|t Frontiers in molecular neuroscience
|v 14
|y 2021
|x 1662-5099
856 4 _ |y OpenAccess
|u https://pub.dzne.de/record/155882/files/DZNE-2021-01042.pdf
856 4 _ |y OpenAccess
|x pdfa
|u https://pub.dzne.de/record/155882/files/DZNE-2021-01042.pdf?subformat=pdfa
909 C O |o oai:pub.dzne.de:155882
|p openaire
|p open_access
|p VDB
|p driver
|p dnbdelivery
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 1
|6 P:(DE-2719)2812366
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 7
|6 P:(DE-2719)2000047
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-352
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Disease Mechanisms
|x 0
914 1 _ |y 2021
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2022-11-29
915 _ _ |a Creative Commons Attribution CC BY (No Version)
|0 LIC:(DE-HGF)CCBYNV
|2 V:(DE-HGF)
|b DOAJ
|d 2021-01-28
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2022-11-29
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2021-01-28
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2022-11-29
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b FRONT MOL NEUROSCI : 2021
|d 2022-11-29
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0501
|2 StatID
|b DOAJ Seal
|d 2021-05-11T12:57:39Z
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2021-01-28
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0500
|2 StatID
|b DOAJ
|d 2021-05-11T12:57:39Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2022-11-29
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2022-11-29
915 _ _ |a OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b DOAJ : Blind peer review
|d 2021-05-11T12:57:39Z
915 _ _ |a Article Processing Charges
|0 StatID:(DE-HGF)0561
|2 StatID
|d 2021-01-28
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b FRONT MOL NEUROSCI : 2021
|d 2022-11-29
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2021-01-28
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1110
|2 StatID
|b Current Contents - Clinical Medicine
|d 2022-11-29
915 _ _ |a Fees
|0 StatID:(DE-HGF)0700
|2 StatID
|d 2021-01-28
920 1 _ |0 I:(DE-2719)1410002
|k AG Fischer
|l Epigenetics and Systems Medicine in Neurodegenerative Diseases
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-2719)1410002
980 1 _ |a FullTexts


LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21