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@ARTICLE{Dehingia:304486,
      author       = {B. Dehingia and M. Milewska-Puchała and M. Janowski and
                      M.-R. Rafiee and M. Abbas and A. Piotrowska and J. Senge and
                      P. Blaut and D. Walsh and J. Severino and D. Chaudhury and
                      S. Iqbal and R. Montiel-Manriquez and S. Jankowska and P.
                      Zare and W. Huber and J. Xu and R. Casellas and T.
                      Zimmermann and P. Dłotko and J. Krijgsveld$^*$ and A.
                      Pękowska},
      title        = {{RNA}-binding proteins mediate the maturation of chromatin
                      topology during differentiation.},
      journal      = {Nature cell biology},
      volume       = {nn},
      issn         = {1465-7392},
      address      = {New York, NY},
      publisher    = {Nature America},
      reportid     = {DKFZ-2025-01878},
      pages        = {nn},
      year         = {2025},
      note         = {epub},
      abstract     = {Topologically associating domains (TADs) and chromatin
                      architectural loops impact promoter-enhancer interactions,
                      with CCCTC-binding factor (CTCF) defining TAD borders and
                      loop anchors. TAD boundaries and loops progressively
                      strengthen upon embryonic stem (ES) cell differentiation,
                      underscoring the importance of chromatin topology in
                      ontogeny. However, the mechanisms driving this process
                      remain unclear. Here we show a widespread increase in
                      CTCF-RNA-binding protein (RBP) interactions upon ES to
                      neural stem (NS) cell differentiation. While dispensable in
                      ES cells, RBPs reinforce CTCF-anchored chromatin topology in
                      NS cells. We identify Pantr1, a non-coding RNA, as a key
                      facilitator of CTCF-RBP interactions, promoting chromatin
                      maturation. Using acute CTCF degradation, we find that,
                      through its insulator function, CTCF helps maintain neuronal
                      gene silencing in NS cells by acting as a barrier to
                      untimely gene activation during development. Altogether, we
                      reveal a fundamental mechanism driving developmentally
                      linked chromatin structural consolidation and the
                      contribution of this process to the control of gene
                      expression in differentiation.},
      cin          = {B230},
      ddc          = {570},
      cid          = {I:(DE-He78)B230-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40921733},
      doi          = {10.1038/s41556-025-01735-5},
      url          = {https://inrepo02.dkfz.de/record/304486},
}