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@ARTICLE{Wischhof:165349,
      author       = {Wischhof, Lena and Lee, Hang-mao and Tutas, Janine and
                      Overkott, Clemens and Tedt, Eileen and Stork, Miriam and
                      Peitz, Michael and Brüstle, Oliver and Ulas, Thomas and
                      Händler, Kristian and Schultze, Joachim L and Ehninger, Dan
                      and Nicotera, Pierluigi and Salomoni, Paolo and Bano,
                      Daniele},
      title        = {{BCL}7{A}-containing {SWI}/{SNF}/{BAF} complexes modulate
                      mitochondrial bioenergetics during neural progenitor
                      differentiation.},
      journal      = {The EMBO journal},
      volume       = {41},
      number       = {23},
      issn         = {0261-4189},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DZNE-2022-01626},
      pages        = {e110595},
      year         = {2022},
      abstract     = {Mammalian SWI/SNF/BAF chromatin remodeling complexes
                      influence cell lineage determination. While the contribution
                      of these complexes to neural progenitor cell (NPC)
                      proliferation and differentiation has been reported, little
                      is known about the transcriptional profiles that determine
                      neurogenesis or gliogenesis. Here, we report that BCL7A is a
                      modulator of the SWI/SNF/BAF complex that stimulates the
                      genome-wide occupancy of the ATPase subunit BRG1. We
                      demonstrate that BCL7A is dispensable for SWI/SNF/BAF
                      complex integrity, whereas it is essential to regulate
                      Notch/Wnt pathway signaling and mitochondrial bioenergetics
                      in differentiating NPCs. Pharmacological stimulation of Wnt
                      signaling restores mitochondrial respiration and attenuates
                      the defective neurogenic patterns observed in NPCs lacking
                      BCL7A. Consistently, treatment with an enhancer of
                      mitochondrial biogenesis, pioglitazone, partially restores
                      mitochondrial respiration and stimulates neuronal
                      differentiation of BCL7A-deficient NPCs. Using conditional
                      BCL7A knockout mice, we reveal that BCL7A expression in NPCs
                      and postmitotic neurons is required for neuronal plasticity
                      and supports behavioral and cognitive performance. Together,
                      our findings define the specific contribution of
                      BCL7A-containing SWI/SNF/BAF complexes to
                      mitochondria-driven NPC commitment, thereby providing a
                      better understanding of the cell-intrinsic transcriptional
                      processes that connect metabolism, neuronal morphogenesis,
                      and cognitive flexibility.},
      keywords     = {Animals / Mice / Adenosine Triphosphatases: metabolism /
                      Chromatin Assembly and Disassembly / Energy Metabolism /
                      Mitochondria: metabolism / Transcription Factors: genetics /
                      Transcription Factors: metabolism / Microfilament Proteins:
                      metabolism / Neural Stem Cells: cytology / Cell
                      Differentiation / BCL7A (Other) / SWI/SNF/BAF complex
                      (Other) / cognitive function (Other) / mitochondrial OXPHOS
                      (Other) / neural progenitor cells (NPCs) (Other)},
      cin          = {AG Bano / AG Salomoni / AG Schultze / AG Ehninger /
                      PRECISE},
      ddc          = {570},
      cid          = {I:(DE-2719)1013003 / I:(DE-2719)1013032 /
                      I:(DE-2719)1013038 / I:(DE-2719)1013005 /
                      I:(DE-2719)1013031},
      pnm          = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
                      (POF4-352) / 354 - Disease Prevention and Healthy Aging
                      (POF4-354)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352 /
                      G:(DE-HGF)POF4-354},
      experiment   = {EXP:(DE-2719)PRECISE-20190321},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC9713712},
      pubmed       = {pmid:36305367},
      doi          = {10.15252/embj.2022110595},
      url          = {https://pub.dzne.de/record/165349},
}