c-Myc is necessary for DNA damage-induced apoptosis in the G(2) phase of the cell cycle.
The c-myc proto-oncogene encodes a transcription factor that participates in the regulation of cellular proliferation, differentiation, and apoptosis. Ectopic overexpression of c-Myc has been shown to sensitize cells to apoptosis. We report here that cells lacking c-Myc activity due to disruption of the c-myc gene by targeted homologous recombination are defective in DNA damage-initiated apoptosis in the G(2) phase of the cell cycle. The downstream effector of c-Myc is cyclin A, whose ectopic expression in c-myc(-/-) cells rescues the apoptosis defect. The kinetics of the G(2) response indicate that the induction of cyclin A and the concomitant activation of Cdk2 represent an early step during commitment to apoptosis. In contrast, expression of cyclins E and D1 does not rescue the apoptosis defect, and apoptotic processes in G(1) phase are not affected in c-myc(-/-) cells. These observations link DNA damage-induced apoptosis with cell cycle progression and implicate c-Myc in the functioning of a subset of these pathways.[1]References
- c-Myc is necessary for DNA damage-induced apoptosis in the G(2) phase of the cell cycle. Adachi, S., Obaya, A.J., Han, Z., Ramos-Desimone, N., Wyche, J.H., Sedivy, J.M. Mol. Cell. Biol. (2001) [Pubmed]
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