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Cyclin F suppresses B-Myb activity to promote cell cycle checkpoint control

Author

Listed:
  • Ditte Kjærsgaard Klein

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

  • Saskia Hoffmann

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

  • Johanna K. Ahlskog

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

  • Karen O’Hanlon

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

  • Marianne Quaas

    (Medical School, University of Leipzig, Semmelweisstr. 14, 04103)

  • Brian D. Larsen

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

  • Baptiste Rolland

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

  • Heike I. Rösner

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

  • David Walter

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

  • Arne Nedergaard Kousholt

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

  • Tobias Menzel

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

  • Michael Lees

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

  • Jens Vilstrup Johansen

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

  • Juri Rappsilber

    (Wellcome Trust Centre for Cell Biology, University of Edinburgh, Michael Swann Building, Kings Buildings, Mayfield Road, Edinburgh EH9 3JR, Scotland)

  • Kurt Engeland

    (Medical School, University of Leipzig, Semmelweisstr. 14, 04103)

  • Claus Storgaard Sørensen

    (Biotech Research and Innovation Centre (BRIC), University of Copenhagen)

Abstract

Cells respond to DNA damage by activating cell cycle checkpoints to delay proliferation and facilitate DNA repair. Here, to uncover new checkpoint regulators, we perform RNA interference screening targeting genes involved in ubiquitylation processes. We show that the F-box protein cyclin F plays an important role in checkpoint control following ionizing radiation. Cyclin F-depleted cells initiate checkpoint signalling after ionizing radiation, but fail to maintain G2 phase arrest and progress into mitosis prematurely. Importantly, cyclin F suppresses the B-Myb-driven transcriptional programme that promotes accumulation of crucial mitosis-promoting proteins. Cyclin F interacts with B-Myb via the cyclin box domain. This interaction is important to suppress cyclin A-mediated phosphorylation of B-Myb, a key step in B-Myb activation. In summary, we uncover a regulatory mechanism linking the F-box protein cyclin F with suppression of the B-Myb/cyclin A pathway to ensure a DNA damage-induced checkpoint response in G2.

Suggested Citation

  • Ditte Kjærsgaard Klein & Saskia Hoffmann & Johanna K. Ahlskog & Karen O’Hanlon & Marianne Quaas & Brian D. Larsen & Baptiste Rolland & Heike I. Rösner & David Walter & Arne Nedergaard Kousholt & Tobia, 2015. "Cyclin F suppresses B-Myb activity to promote cell cycle checkpoint control," Nature Communications, Nature, vol. 6(1), pages 1-11, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms6800
    DOI: 10.1038/ncomms6800
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