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@ARTICLE{Feurle:155832,
      author       = {Feurle, Patrick and Abentung, Andreas and Cera, Isabella
                      and Wahl, Nico and Ablinger, Cornelia and Bucher, Michael
                      and Stefan, Eduard and Sprenger, Simon and Teis, David and
                      Fischer, Andre and Laighneach, Aodán and Whitton, Laura and
                      Morris, Derek W and Apostolova, Galina and Dechant, Georg},
      title        = {{SATB}2-{LEMD}2 interaction links nuclear shape plasticity
                      to regulation of cognition-related genes.},
      journal      = {The EMBO journal},
      volume       = {40},
      number       = {3},
      issn         = {1460-2075},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DZNE-2021-00992},
      pages        = {e103701},
      year         = {2021},
      abstract     = {SATB2 is a schizophrenia risk gene and is genetically
                      associated with human intelligence. How it affects cognition
                      at molecular level is currently unknown. Here, we show that
                      interactions between SATB2, a chromosomal scaffolding
                      protein, and the inner nuclear membrane protein LEMD2
                      orchestrate the response of pyramidal neurons to neuronal
                      activation. Exposure to novel environment in vivo causes
                      changes in nuclear shape of CA1 hippocampal neurons via a
                      SATB2-dependent mechanism. The activity-driven plasticity of
                      the nuclear envelope requires not only SATB2, but also its
                      protein interactor LEMD2 and the ESCRT-III/VPS4
                      membrane-remodeling complex. Furthermore, LEMD2 depletion in
                      cortical neurons, similar to SATB2 ablation, affects
                      neuronal activity-dependent regulation of multiple rapid and
                      delayed primary response genes. In human genetic data,
                      LEMD2-regulated genes are enriched for de novo mutations
                      reported in intellectual disability and schizophrenia and
                      are, like SATB2-regulated genes, enriched for common
                      variants associated with schizophrenia and cognitive
                      function. Hence, interactions between SATB2 and the inner
                      nuclear membrane protein LEMD2 influence gene expression
                      programs in pyramidal neurons that are linked to cognitive
                      ability and psychiatric disorder etiology.},
      keywords     = {ATPases Associated with Diverse Cellular Activities:
                      metabolism / Animals / Cell Nucleus: metabolism / Cell
                      Plasticity / Cells, Cultured / Cognition / Endosomal Sorting
                      Complexes Required for Transport: metabolism / Gene
                      Regulatory Networks / HeLa Cells / Hippocampus: cytology /
                      Hippocampus: metabolism / Humans / Intellectual Disability:
                      genetics / Intellectual Disability: metabolism / Male /
                      Matrix Attachment Region Binding Proteins: chemistry /
                      Matrix Attachment Region Binding Proteins: genetics / Matrix
                      Attachment Region Binding Proteins: metabolism / Membrane
                      Proteins: chemistry / Membrane Proteins: genetics / Membrane
                      Proteins: metabolism / Mice / Mutation / Neurons: cytology /
                      Neurons: metabolism / Nuclear Envelope: metabolism / Nuclear
                      Proteins: chemistry / Nuclear Proteins: genetics / Nuclear
                      Proteins: metabolism / Schizophrenia: genetics /
                      Schizophrenia: metabolism / Transcription Factors: chemistry
                      / Transcription Factors: genetics / Transcription Factors:
                      metabolism / Vacuolar Proton-Translocating ATPases:
                      metabolism / SATB2 (Other) / chromatin (Other) / human
                      cognitive ability (Other) / neuronal activity (Other) /
                      nuclear envelope (Other)},
      cin          = {AG Fischer},
      ddc          = {570},
      cid          = {I:(DE-2719)1410002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33319920},
      pmc          = {pmc:PMC7849313},
      doi          = {10.15252/embj.2019103701},
      url          = {https://pub.dzne.de/record/155832},
}