Cyclin E is stabilized in response to replication fork barriers leading to prolonged S phase arrest

J Biol Chem. 2009 Dec 18;284(51):35325-37. doi: 10.1074/jbc.M109.035949.

Abstract

Cyclin E is a regulator of cyclin-dependent protein kinases (Cdks) and is involved in mediating the cell cycle transition from G(1) to S phase. Here, we describe a novel function for cyclin E in the long term maintenance of checkpoint arrest in response to replication barriers. Exposure of cells to mitomycin C or UV irradiation, but not ionizing radiation, induces stabilization of cyclin E. Stabilization of cyclin E reduces the activity of Cdk2-cyclin A, resulting in a slowing of S phase progression and arrest. In addition, cyclin E is shown to be required for stabilization of Cdc6, which is required for activation of Chk1 and the replication checkpoint pathway. Furthermore, the stabilization of cyclin E in response to replication fork barriers depends on ATR, but not Nbs1 or Chk1. These results indicate that in addition to its well studied role in promoting cell cycle progression, cyclin E also has a role in regulating cell cycle arrest in response to DNA damage.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Ataxia Telangiectasia Mutated Proteins
  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / metabolism
  • Checkpoint Kinase 1
  • Cyclin A / genetics
  • Cyclin A / metabolism
  • Cyclin E / metabolism*
  • Cyclin-Dependent Kinase 2 / metabolism
  • DNA Damage / drug effects
  • DNA Damage / physiology
  • DNA Damage / radiation effects
  • DNA Replication / drug effects
  • DNA Replication / physiology*
  • DNA Replication / radiation effects
  • G1 Phase / drug effects
  • G1 Phase / physiology
  • G1 Phase / radiation effects
  • HeLa Cells
  • Humans
  • Mitomycin / pharmacology
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism
  • Nucleic Acid Synthesis Inhibitors / pharmacology
  • Protein Kinases / genetics
  • Protein Kinases / metabolism
  • Protein Serine-Threonine Kinases / metabolism
  • Protein Stability / drug effects
  • Protein Stability / radiation effects
  • S Phase / drug effects
  • S Phase / physiology*
  • S Phase / radiation effects
  • Ultraviolet Rays

Substances

  • CDC6 protein, human
  • Cell Cycle Proteins
  • Cyclin A
  • Cyclin E
  • NBN protein, human
  • Nuclear Proteins
  • Nucleic Acid Synthesis Inhibitors
  • Mitomycin
  • Protein Kinases
  • ATR protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • CHEK1 protein, human
  • Checkpoint Kinase 1
  • Protein Serine-Threonine Kinases
  • CDK2 protein, human
  • Cyclin-Dependent Kinase 2