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DNA damage response mechanisms trigger cell-cycle arrest, and attempt to repair DNA lesions or promote cell death/senescence if repair is not possible. Replication stress is observed in preneoplastic cells due to increased proliferation signals from oncogenic mutations.
Depending on the extent of injury, the cellular response may be adaptive and where possible, homeostasis is restored. [1] Cell death occurs when the severity of the injury exceeds the cell's ability to repair itself. [2] Cell death is relative to both the length of exposure to a harmful stimulus and the severity of the damage caused. [1]
Most damage can be repaired without triggering the damage response system, however more complex damage activates ATR and ATM, key protein kinases in the damage response system. [92] DNA damage inhibits M-CDKs which are a key component of progression into mitosis. In all eukaryotic cells, ATR and ATM are protein kinases that detect DNA damage.
This supports a model where phosphorylation by rad3 causes recruitment of these proteins to sites of DNA damage where they mediate the activity of DNA polymerases involved in DNA repair. [1] The main rad3 effector is the kinase Chk1, which is required for the G2-M arrest in response to DNA-damaging agents. [9]
In terms of repair models in the cell cycle, HR is only possible during the S and G2 phases, while NHEJ can occur throughout whole process. [3] These repair pathways are all regulated by the overarching DNA damage response mechanism. [4] Besides HR and NHEJ, there are also other repair models which exists in cells.
Nucleotide excision repair is a DNA repair mechanism. [2] DNA damage occurs constantly because of chemicals (e.g. intercalating agents), radiation and other mutagens. Three excision repair pathways exist to repair single stranded DNA damage: Nucleotide excision repair (NER), base excision repair (BER), and DNA mismatch repair (MMR).
When DNA damage occurs, or when the cell detects any defects which necessitate it to delay or halt the cell cycle in G1, arrest occurs through several mechanisms. The rapid response involves phosphorylation events that initiate with either kinase ATM ( Ataxia telangiectasia mutated ) or ATR ( Ataxia Telangiectasia and Rad3 related ), which act ...
Degradation of nuclear DNA into nucleosomal units is one of the hallmarks of apoptotic cell death. It occurs in response to various apoptotic stimuli in a wide variety of cell types. Molecular characterization of this process identified a specific DNase (CAD, caspase-activated DNase) that cleaves chromosomal DNA in a caspase-dependent manner.