Analysis of cell cycle progression following DNA damage A The Biology Diagrams Genome damage is a threat to all organisms. To respond to such damage, DNA damage responses (DDRs) lead to cell cycle arrest, DNA repair, and cell death. Many DDR components are highly conserved, whereas others have adapted to specific organismal needs. Immense progress in this field has been driven by model genetic organism research. DNA damage checkpoints were initially defined as non-essential regulatory pathways that control the ability of cells to arrest the cell cycle in response to DNA damage, allowing time for repair.
The CDKNs not only act as cell cycle checkpoints but also are heavily linked to DNA damage response. For instance, P53 is a tumor suppressor gene and responsible for regulating genome stability. In response to DNA double-strand breaks (DSB), P53 can directly activate the ataxia-telangiectasia mutated (ATM) kinase through phosphorylation.
DNA Damage Response and Cell Cycle Regulation in Pluripotent Stem Cells ... Biology Diagrams
Upon the generation of a DNA lesion, the DDR coordinates the response by activating two parallel routes: (1) the DNA damage checkpoint, a cell cycle blockage that restrains chromosome segregation until the damaged DNA has been fixed, and (2) the stimulation of a set of DNA repair factors that deal with the restoration of the broken DNA.
DNA damage response and the cell cycle are two intertwined cellular processes. On the one hand, as discussed above, DDR leads to cell cycle arrest by activating checkpoint kinases. On the other hand, an emerging idea is that even the unperturbed cell cycle has a constitutive surveillance mechanism that is related to DDR [24, 25]. This is
The DNA damage response: putting checkpoints in perspective Biology Diagrams
To combat this threat, eukaryotic cells have evolved a set of sophisticated molecular mechanisms that are collectively known as the DNA damage response (DDR). This surveillance system controls several aspects of the cellular response, including the detection of lesions, a temporary cell cycle arrest, and the repair of the broken DNA.
