G2/M Checkpoint
In vertebrate cells, the G2/M DNA damage checkpoint consists of an arrest of the cell in G2 just before mitotic entry in response to genotoxic stress (such as UV radiation, oxidative stress, DNA intercalating agents, etc.) in both a p53-dependent and p53-independent manner. DNA damage signals cause activation of the transcription factor p53. CDK1 is directly inhibited by three transcriptional targets of p53: p21, Gadd45, and 14-3-3σ. Inactive Cyclin B1/CDK1 is sequestered in the nucleus by p21, while active Cyclin B1/CDK1 complexes are sequestered in the cytoplasm by 14-3-3σ. Gadd45 disrupts the binding of Cyclin B1 and CDK1 through direct interaction with CDK1. P53 also transcriptionally represses CDK1.
P53-independent G2 arrest is mainly affected through the actions of Chk1 kinase. DNA damage is sensed by ATM and ATR (Rad3 and Mec1 in yeast), which then signal to Chk1 and Chk2. Chk1 then mediates the degradation of cdc25A, an activator of CDK1. ATR/ATM also activate p53, indicating that these pathways may act synergistically in regulating G2 arrest.
Both p53-dependent and p53-independent cell cycle arrest are not specific to G2; these same proteins function upstream in DNA damage checkpoints in G1 and S phase as well. In yeast, which has no p53 homolog, G2 arrest functions through the p53-independent pathway.
Read more about this topic: G2 Phase