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@ARTICLE{Tolve:162865,
      author       = {Tolve, Marianna and Ulusoy, Ayse and Patikas, Nikolaos and
                      Islam, K Ushna S and Bodea, Gabriela O and Öztürk, Ece and
                      Broske, Bianca and Mentani, Astrid and Wagener, Antonia and
                      van Loo, Karen M J and Britsch, Stefan and Liu, Pengtao and
                      Khaled, Walid T and Metzakopian, Emmanouil and Baader,
                      Stephan L and Di Monte, Donato A and Blaess, Sandra},
      title        = {{T}he transcription factor {BCL}11{A} defines distinct
                      subsets of midbrain dopaminergic neurons.},
      journal      = {Cell reports},
      volume       = {36},
      number       = {11},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2021-01520},
      pages        = {109697},
      year         = {2021},
      note         = {CC BY-NC-ND},
      abstract     = {Midbrain dopaminergic (mDA) neurons are diverse in their
                      projection targets, effect on behavior, and susceptibility
                      to neurodegeneration. Little is known about the molecular
                      mechanisms establishing this diversity during development.
                      We show that the transcription factor BCL11A is expressed in
                      a subset of mDA neurons in the developing and adult murine
                      brain and in a subpopulation of
                      pluripotent-stem-cell-derived human mDA neurons. By
                      combining intersectional labeling and viral-mediated
                      tracing, we demonstrate that Bcl11a-expressing mDA neurons
                      form a highly specific subcircuit within the murine
                      dopaminergic system. In the substantia nigra, the
                      Bcl11a-expressing mDA subset is particularly vulnerable to
                      neurodegeneration upon α-synuclein overexpression or
                      oxidative stress. Inactivation of Bcl11a in murine mDA
                      neurons increases this susceptibility further, alters the
                      distribution of mDA neurons, and results in deficits in
                      skilled motor behavior. In summary, BCL11A defines mDA
                      subpopulations with highly distinctive characteristics and
                      is required for establishing and maintaining their normal
                      physiology.},
      keywords     = {Animals / Behavior, Animal / Brain: metabolism / Dopamine:
                      metabolism / Dopaminergic Neurons: metabolism / Humans /
                      Induced Pluripotent Stem Cells: cytology / Induced
                      Pluripotent Stem Cells: metabolism / Male / Mice / Mice,
                      Knockout / Repressor Proteins: deficiency / Repressor
                      Proteins: genetics / Repressor Proteins: metabolism /
                      Substantia Nigra: metabolism / Substantia Nigra: pathology /
                      Transcriptome / Ventral Tegmental Area: metabolism / Ventral
                      Tegmental Area: pathology / alpha-Synuclein: genetics /
                      alpha-Synuclein: metabolism / alpha-synuclein (Other) /
                      behavior (Other) / circuits (Other) / development (Other) /
                      dopaminergic neurons (Other) / iPSCs (Other) / mouse (Other)
                      / neurodegeneration (Other) / neuronal diversity (Other) /
                      transcription factor (Other)},
      cin          = {AG Di Monte},
      ddc          = {610},
      cid          = {I:(DE-2719)1013008},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34525371},
      doi          = {10.1016/j.celrep.2021.109697},
      url          = {https://pub.dzne.de/record/162865},
}