What happens when DNA damage is detected during the G2 phase?

The G₂ phase is the final part of interphase in the cell cycle. In this phase, the cell prepares itself to enter mitosis. One of the main roles of this phase is to check if the DNA, which was copied in the S phase, is complete and without any mistake. For this purpose, the cell uses a control system called the G₂ DNA damage checkpoint.

This checkpoint works like a security checking system. It stays active during the G₂ phase and keeps watching the DNA. If it finds any kind of damage in the DNA, such as breaks or errors, it immediately stops the cell from entering mitosis. This process is very important because if a cell enters mitosis with damaged DNA, it will pass those mistakes to the daughter cells. These mistakes can lead to serious problems like cancer or cell death.

So, when DNA damage is detected by the G₂ checkpoint, it sends signals inside the cell. These signals stop the proteins that are responsible for starting mitosis. As a result, the cell stays in the G₂ phase and does not move forward. This pause gives the cell enough time to repair the damaged DNA using special repair systems. If the DNA is successfully repaired, the cell continues to mitosis. But if the damage is too much and cannot be fixed, the cell goes for programmed cell death, which is called apoptosis. This system helps the body to remove damaged cells and maintain healthy tissue.

Sequence of Events After DNA Damage Detection in G₂ Phase

The process begins when the cell detects DNA damage, commonly in the form of double-strand breaks (DSBs) or replication stress. This damage is sensed by the ATM (Ataxia Telangiectasia Mutated) and ATR (ATM and Rad3-related) proteins. ATM primarily responds to DSBs while ATR responds to a broader range of DNA abnormalities.

Upon activation, ATM and ATR phosphorylate downstream checkpoint kinases, mainly Chk1 and Chk2. These kinases then inhibit the activity of Cdc25C phosphatase by phosphorylation. Cdc25C is responsible for activating the Cdk1–Cyclin B complex, which is essential for initiating mitosis. When Cdc25C is inactivated, Cdk1–Cyclin B remains inactive, leading to a cell cycle arrest at the G₂ phase.

During this arrest, the cell utilizes its DNA repair machinery, such as homologous recombination repair, to correct the damage. If the repair is successful, Cdc25C gets reactivated, the Cdk1–Cyclin B complex becomes active and the cell proceeds to mitosis.

However, if the DNA damage cannot be repaired by the cell, the checkpoint leads to activation of p53, a tumor suppressor protein. Stabilized p53 then initiates transcription of pro-apoptotic genes like BAX, PUMA and others, resulting in apoptosis. This ensures that genetically unstable cells do not survive or propagate mutations.

Thus, the detection of DNA damage during G₂ triggers a sequence of molecular controls that temporarily halt cell cycle progression, promote repair and eliminate the cell if repair fails. This mechanism is essential for the maintenance of genomic integrity and prevention of tumor development.






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