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Interphase is the active portion of the cell cycle that includes the G1, S, and G2 phases, where the cell grows, replicates its DNA, and prepares for mitosis, respectively. Interphase was formerly called the " resting phase ," but the cell in interphase is not simply dormant .
The eukaryotic cell cycle consists of four distinct phases: G 1 phase, S phase (synthesis), G 2 phase (collectively known as interphase) and M phase (mitosis and cytokinesis). M phase is itself composed of two tightly coupled processes: mitosis, in which the cell's nucleus divides, and cytokinesis, in which the cell's cytoplasm and cell membrane divides forming two daughter cells.
After R and before S, the cell is known as being in G 1-ps, or the pre S phase interval of the G 1 phase. [ 4 ] In order for the cell to continue through the G 1 -pm, there must be a high amount of growth factors and a steady rate of protein synthesis, otherwise the cell will move into G 0 phase.
The G1/S transition is a stage in the cell cycle at the boundary between the G1 phase, in which the cell grows, and the S phase, during which DNA is replicated. [1] It is governed by cell cycle checkpoints to ensure cell cycle integrity and the subsequent S phase can pause in response to improperly or partially replicated DNA. [ 2 ]
Cyclin B1 levels are suppressed throughout G1 and S phases by the anaphase-promoting complex (APC), an E3 ubiquitin ligase which targets cyclin B1 for proteolysis. Transcription begins at the end of S phase after DNA replication, in response to phosphorylation of transcription factors such as NF-Y , FoxM1 and B-Myb by upstream G1 and G1/S ...
The G1/S checkpoint, G2/M checkpoint, and the checkpoint between metaphase and anaphase all monitor for DNA damage and halt cell division by inhibiting different cyclin-CDK complexes. The p53 tumor-suppressor protein plays a crucial role at the G1/S checkpoint and the G2/M checkpoint. Activated p53 proteins result in the expression of many ...
Homologous recombination, an accurate process for repairing DNA double-strand breaks, is most active in S phase, declines in G2/M and is nearly absent in G1 phase. [13] In addition to these canonical checkpoints, recent evidence suggests that abnormalities in histone supply and nucleosome assembly can also alter S-phase progression. [14]
The G1/S transition is regulated by cyclin E binding to Cdk2 which phosphorylates Rb as well (Merrick and Fisher, 2011). S phase is then driven by the binding of cyclin A with Cdk2. In late S phase, cyclin A binds with Cdk1 to promote late replication origins and also initiates the condensation of the chromatin in the late G2 phase.