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@ARTICLE{VegaSendino:289078,
      author       = {M. Vega-Sendino and F. F. Lüttmann and T. Olbrich and Y.
                      Chen and C. Kuenne and P. Stein and D. Tillo and G. I. Carey
                      and J. Zhong$^*$ and V. Savy and L. Radonova and T. Lu and
                      B. Saykali and K.-P. Kim and C. N. Domingo and L. Schüler
                      and S. Günther and M. Bentsen and D. Bosnakovski and H.
                      Schöler and M. Kyba and T. K. Maity and L. M. Jenkins and
                      M. Looso and C. J. Williams and J. Kim and S. Ruiz},
      title        = {{T}he homeobox transcription factor {DUXBL} controls exit
                      from totipotency.},
      journal      = {Nature genetics},
      volume       = {56},
      number       = {4},
      issn         = {1061-4036},
      address      = {London},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DKFZ-2024-00578},
      pages        = {697-709},
      year         = {2024},
      note         = {2024 Apr;56(4):697-709},
      abstract     = {In mice, exit from the totipotent two-cell (2C) stage
                      embryo requires silencing of the 2C-associated
                      transcriptional program. However, the molecular mechanisms
                      involved in this process remain poorly understood. Here we
                      demonstrate that the 2C-specific transcription factor double
                      homeobox protein (DUX) mediates an essential negative
                      feedback loop by inducing the expression of DUXBL to promote
                      this silencing. We show that DUXBL gains accessibility to
                      DUX-bound regions specifically upon DUX expression.
                      Furthermore, we determine that DUXBL interacts with TRIM24
                      and TRIM33, members of the TRIM superfamily involved in gene
                      silencing, and colocalizes with them in nuclear foci upon
                      DUX expression. Importantly, DUXBL overexpression impairs
                      2C-associated transcription, whereas Duxbl inactivation in
                      mouse embryonic stem cells increases DUX-dependent induction
                      of the 2C-transcriptional program. Consequently, DUXBL
                      deficiency in embryos results in sustained expression of
                      2C-associated transcripts leading to early developmental
                      arrest. Our study identifies DUXBL as an essential regulator
                      of totipotency exit enabling the first divergence of cell
                      fates.},
      cin          = {B400},
      ddc          = {570},
      cid          = {I:(DE-He78)B400-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38509386},
      doi          = {10.1038/s41588-024-01692-z},
      url          = {https://inrepo02.dkfz.de/record/289078},
}