The cell cycle consists of four distinct and ordered phases, termed G0/G1 (gap 1), S (DNA synthesis), G2 (gap 2), and M (mitosis). The cell cycle process is highly conserved and precisely controlled to govern the genome duplication and separation into the daughter cells. In multicellular organisms, the response to DNA damage can result in two major physiological consequences: (1) Cells can undergo cell cycle arrest, repair the damage and re-enter the cell cycle, or (2) cells can be targeted for cell death (apoptosis) and removed from the population. The sensor phase recognizes the damage and activates the signal transduction phase to block cell cycle progression and select the appropriate repair pathway. Within cells, multiple pathways contribute to DNA repair, but independent of the specific repair pathway involved, three phases of checkpoint activation are traditionally identified: (1) Sensing of damage, (2) Activating the signaling cascade, and (3) Switching on downstream effectors. Once the damaged DNA is repaired, the checkpoint machinery triggers signals that will resume cell cycle progression. Checkpoints are induced to delay cell cycle progression and to allow cells time to repair damaged DNA prior to DNA replication. DNA damage checkpoints have been functionally conserved throughout eukaryotic evolution, with most of the relevant players in the checkpoint response highly conserved from yeast to humans. However, regardless of the type of damage a sophisticated surveillance mechanism, that elicits DNA damage checkpoints, detects and signals its presence to the DNA repair machinery. To preserve genome integrity, eukaryotic cells have evolved repair mechanisms specific for different types of DNA Damage. Genetic damage produced by either exogenous or endogenous mechanisms represents an ongoing threat to the cell. As described in this section, the cell cycle checkpoint has another critical function in response to cellular stress and DNA damage. In the previous section, we learn how the cell cycle checkpoint allows timely progression of the cell cycle in undamaged cells.
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