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c-Myc is necessary for DNA damage-induced apoptosis in the G(2) phase of the cell cycle

S Adachi1, A J Obaya, Z Han

  • 1Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 02912, USA.

Molecular and Cellular Biology
|July 5, 2001
PubMed

Insights

Cells lacking c-Myc activity are defective in DNA damage-initiated apoptosis. Ectopic expression of cyclin A rescues this defect, linking c-Myc to cell cycle-regulated apoptosis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • The c-myc proto-oncogene encodes a transcription factor regulating cell proliferation, differentiation, and apoptosis.
  • Ectopic overexpression of c-Myc sensitizes cells to apoptosis.

Purpose of the Study:

  • To investigate the role of c-Myc in DNA damage-induced apoptosis.
  • To identify downstream effectors of c-Myc involved in apoptosis regulation.

Main Methods:

  • Targeted homologous recombination to disrupt the c-myc gene.
  • Analysis of apoptosis in c-myc deficient cells.
  • Ectopic expression of cyclins (A, E, D1) to assess rescue of apoptosis defects.

Main Results:

  • c-myc(-/-) cells exhibit defective G(2) phase apoptosis following DNA damage.
  • Ectopic expression of cyclin A rescues the apoptosis defect in c-myc(-/-) cells.
  • Cyclin A induction and Cdk2 activation are early events in apoptosis commitment.
  • Cyclins E and D1 do not rescue the defect; G(1) phase apoptosis is unaffected.

Conclusions:

  • c-Myc is crucial for DNA damage-induced apoptosis in the G(2) cell cycle phase.
  • Cyclin A acts as a downstream effector of c-Myc in this apoptotic pathway.
  • c-Myc links DNA damage response, cell cycle progression, and apoptosis.

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