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Nuclear and cytosolic fractions of SOX2 synergize as transcriptional and translational co-regulators of cell fate.
Schaefer, Thorsten; Mittal, Nitish; Wang, Hui; Ataman, Meric; Candido, Silvia; Lötscher, Jonas; Velychko, Sergiy; Tintignac, Lionel; Bock, Thomas; Börsch, Anastasiya; Baßler, Jochen; Rao, Tata Nageswara; Zmajkovic, Jakub; Roffeis, Sarah; Löliger, Jordan; Jacob, Francis; Dumlin, Alain; Schürch, Christoph; Schmidt, Alexander; Skoda, Radek C; Wymann, Matthias P; Hess, Christoph; Schöler, Hans R; Zaehres, Holm; Hurt, Ed; Zavolan, Mihaela; Lengerke, Claudia.
Afiliação
  • Schaefer T; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland. Electronic address: thorsten.schaefer@unibas.ch.
  • Mittal N; Biozentrum, University of Basel, Basel, Switzerland.
  • Wang H; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland; Shanghai University of Medicine and Health Sciences, Shanghai, China.
  • Ataman M; Biozentrum, University of Basel, Basel, Switzerland.
  • Candido S; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland.
  • Lötscher J; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland.
  • Velychko S; Max Planck Institute for Molecular Biomedicine, Münster, Germany; Department of Genetics, Harvard Medical School, Boston, MA, USA.
  • Tintignac L; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland.
  • Bock T; Proteomics Core Facility, Biozentrum, University of Basel, Basel, Switzerland.
  • Börsch A; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland.
  • Baßler J; Biochemistry Center Heidelberg, Heidelberg University, Heidelberg, Germany.
  • Rao TN; Medical Research Center, Department of Medical Oncology and Hematology, Cantonal Hospital St. Gallen, St. Gallen, Switzerland; Institute of Pharmacology, University of Bern, Bern, Switzerland.
  • Zmajkovic J; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland; Research Institute of Molecular Pathology (IMP), Vienna, Austria.
  • Roffeis S; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland.
  • Löliger J; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland.
  • Jacob F; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland.
  • Dumlin A; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland.
  • Schürch C; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland.
  • Schmidt A; Proteomics Core Facility, Biozentrum, University of Basel, Basel, Switzerland.
  • Skoda RC; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland.
  • Wymann MP; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland.
  • Hess C; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland; CITIID, Department of Medicine, University of Cambridge, Cambridge, UK.
  • Schöler HR; Max Planck Institute for Molecular Biomedicine, Münster, Germany.
  • Zaehres H; Max Planck Institute for Molecular Biomedicine, Münster, Germany; Institute of Anatomy, Ruhr University Bochum, Bochum, Germany.
  • Hurt E; Biochemistry Center Heidelberg, Heidelberg University, Heidelberg, Germany.
  • Zavolan M; Biozentrum, University of Basel, Basel, Switzerland.
  • Lengerke C; Department of Biomedicine, University of Basel and University Hospital Basel, Basel, Switzerland; Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Cell Rep ; 43(10): 114807, 2024 Oct 03.
Article em En | MEDLINE | ID: mdl-39368083
ABSTRACT
Stemness and pluripotency are mediated by transcriptional master regulators that promote self-renewal and repress cell differentiation, among which is the high-mobility group (HMG) box transcription factor SOX2. Dysregulated SOX2 expression, by contrast, leads to transcriptional aberrations relevant to oncogenic transformation, cancer progression, metastasis, therapy resistance, and relapse. Here, we report a post-transcriptional mechanism by which the cytosolic pool of SOX2 contributes to these events in an unsuspected manner. Specifically, a low-complexity region within SOX2's C-terminal segment connects to the ribosome to modulate the expression of cognate downstream factors. Independent of nuclear structures or DNA, this C-terminal functionality alone changes metabolic properties and induces non-adhesive growth when expressed in the cytosol of SOX2 knockout cells. We thus propose a revised model of SOX2 action where nuclear and cytosolic fractions cooperate to impose cell fate decisions via both transcriptional and translational mechanisms.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Cell Rep / Cell reports Ano de publicação: 2024 Tipo de documento: Article País de publicação: Estados Unidos
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Cell Rep / Cell reports Ano de publicação: 2024 Tipo de documento: Article País de publicação: Estados Unidos