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

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, Tobias Menzel, Michael Lees, Jens Vilstrup Johansen, Juri Rappsilber, Kurt Engeland and Claus Storgaard Sørensen ()
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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

Nature Communications, 2015, vol. 6, issue 1, 1-11

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms6800

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