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@ARTICLE{Sokpor:155882,
      author       = {Sokpor, Godwin and Kerimoglu, Cemil and Nguyen, Huong and
                      Pham, Linh and Rosenbusch, Joachim and Wagener, Robin and
                      Nguyen, Huu Phuc and Fischer, Andre and Staiger, Jochen F
                      and Tuoc, Tran},
      title        = {{L}oss of {BAF} {C}omplex in {D}eveloping {C}ortex
                      {P}erturbs {R}adial {N}euronal {M}igration in a {WNT}
                      {S}ignaling-{D}ependent {M}anner.},
      journal      = {Frontiers in molecular neuroscience},
      volume       = {14},
      issn         = {1662-5099},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {DZNE-2021-01042},
      pages        = {687581},
      year         = {2021},
      abstract     = {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.},
      keywords     = {BAF complex (Other) / Wnt signaling (Other) / cell adhesion
                      (Other) / cortical development (Other) / cortical lamination
                      (Other) / glial fibers (Other) / neuronal migration (Other)},
      cin          = {AG Fischer},
      ddc          = {610},
      cid          = {I:(DE-2719)1410002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34220450},
      pmc          = {pmc:PMC8243374},
      doi          = {10.3389/fnmol.2021.687581},
      url          = {https://pub.dzne.de/record/155882},
}