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E2f1–3 switch from activators in progenitor cells to repressors in differentiating cells

Author

Listed:
  • Jean-Leon Chong

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

  • Pamela L. Wenzel

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA
    Present address: Division of Pediatric Hematology/Oncology, Children’s Hospital Boston; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA.)

  • M. Teresa Sáenz-Robles

    (University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA)

  • Vivek Nair

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

  • Antoney Ferrey

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

  • John P. Hagan

    (Immunology and Medical Genetics, College of Medicine
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

  • Yorman M. Gomez

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

  • Nidhi Sharma

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

  • Hui-Zi Chen

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

  • Madhu Ouseph

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

  • Shu-Huei Wang

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

  • Prashant Trikha

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

  • Brian Culp

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

  • Louise Mezache

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

  • Douglas J. Winton

    (Cambridge Research Institute, Li Ka Shing Centre, Cambridge CB2 0RE, UK)

  • Owen J. Sansom

    (The Beatson Institute for Cancer Research)

  • Danian Chen

    (Toronto Western Research Institute, University Health Network, and Laboratory Medicine and Pathobiology, University of Toronto)

  • Rod Bremner

    (Toronto Western Research Institute, University Health Network, and Laboratory Medicine and Pathobiology, University of Toronto)

  • Paul G. Cantalupo

    (University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA)

  • Michael L. Robinson

    (Miami University, Oxford, Ohio 45056, USA)

  • James M. Pipas

    (University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA)

  • Gustavo Leone

    (Immunology and Medical Genetics, College of Medicine
    College of Biological Sciences
    Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA)

Abstract

E2f transcription factors The in vivo function of E2f transcription factors has been a matter of debate. Here it is shown that E2f1–3 contribute to the activation of cell cycle genes in dividing progenitor cells during mouse development but are dispensable for cell division. However, in differentiating cells, E2f1–3 act as repressors to facilitate cell cycle exit.

Suggested Citation

  • Jean-Leon Chong & Pamela L. Wenzel & M. Teresa Sáenz-Robles & Vivek Nair & Antoney Ferrey & John P. Hagan & Yorman M. Gomez & Nidhi Sharma & Hui-Zi Chen & Madhu Ouseph & Shu-Huei Wang & Prashant Trikh, 2009. "E2f1–3 switch from activators in progenitor cells to repressors in differentiating cells," Nature, Nature, vol. 462(7275), pages 930-934, December.
    • Handle: RePEc:nat:nature:v:462:y:2009:i:7275:d:10.1038_nature08677
    DOI: 10.1038/nature08677
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    Cited by:

    1. Ryan J. Smith & Hongpan Zhang & Shengen Shawn Hu & Theodora Yung & Roshane Francis & Lilian Lee & Mark W. Onaitis & Peter B. Dirks & Chongzhi Zang & Tae-Hee Kim, 2022. "Single-cell chromatin profiling of the primitive gut tube reveals regulatory dynamics underlying lineage fate decisions," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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