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

Ditte Kjærsgaard Klein1, Saskia Hoffmann1, Johanna K Ahlskog1

  • 1Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Ole Maaløes Vej 5, 2200 Copenhagen N, Denmark.

Nature Communications
|January 6, 2015
PubMed

Insights

The F-box protein cyclin F is crucial for maintaining the G2 cell cycle arrest after DNA damage. Cyclin F depletion causes premature entry into mitosis, highlighting its role in DNA damage checkpoint control.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Cell cycle checkpoints are essential for responding to DNA damage, enabling repair before cell division.
  • Ubiquitylation pathways are increasingly recognized for their roles in regulating cellular processes, including checkpoint control.

Purpose of the Study:

  • To identify novel regulators of DNA damage-induced cell cycle checkpoints.
  • To investigate the role of ubiquitylation factors in checkpoint control following ionizing radiation.

Main Methods:

  • RNA interference (RNAi) screening of ubiquitylation-related genes.
  • Analysis of cell cycle progression and checkpoint signaling after ionizing radiation in cyclin F-depleted cells.
  • Investigation of protein-protein interactions and phosphorylation events involving cyclin F, B-Myb, and cyclin A.

Main Results:

  • Cyclin F is identified as a key regulator of the G2 DNA damage checkpoint.
  • Depletion of cyclin F leads to a failure in maintaining G2 arrest and premature entry into mitosis post-ionizing radiation.
  • Cyclin F suppresses the B-Myb transcriptional program, preventing the accumulation of mitosis-promoting proteins.
  • Cyclin F interacts with B-Myb, inhibiting cyclin A-mediated phosphorylation and activation of B-Myb.

Conclusions:

  • A novel regulatory mechanism involving cyclin F in DNA damage response is uncovered.
  • Cyclin F ensures proper G2 checkpoint maintenance by suppressing the B-Myb/cyclin A pathway.
  • This finding provides new insights into the molecular basis of cell cycle control following DNA damage.

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