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Steps of the cell cycle. The G 2-M checkpoint occurs between the G 2 and M phases. G2-M arrest. The G 2-M DNA damage checkpoint is an important cell cycle checkpoint in eukaryotic organisms that ensures that cells don't initiate mitosis until damaged or incompletely replicated DNA is sufficiently repaired.
The resultant Cdk1 activity also activates expression of Mem1-Fkh, a G2/M transition gene. [19] The rapid surge in cyclin B-Cdk1 activity is necessary, as M phase initiation is an all-or-nothing event engaging in hysteresis. Hysteresis of Cdk1 activity via cyclin B drives M phase entry by establishing a minimum threshold of cyclin B concentration.
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.
Checkpoint kinase 1, commonly referred to as Chk1, is a serine/threonine-specific protein kinase that, in humans, is encoded by the CHEK1 gene. [ 5 ] [ 6 ] Chk1 coordinates the DNA damage response (DDR) and cell cycle checkpoint response. [ 7 ]
These DNA breaks must be repaired before metaphase I. and these DSBs must be repaired before metaphase I. The cell monitor these DSBs via ATM pathway, in which Cdc25 is suppressed when DSB lesion is detected. This pathway is the same as classical DNA damage response and is the part we know the best in meiotic recombination checkpoint.
Cell synchronization is a process by which cells in a culture at different stages of the cell cycle are brought to the same phase. Cell synchrony is a vital process in the study of cells progressing through the cell cycle as it allows population-wide data to be collected rather than relying solely on single-cell experiments.
Cyclin A2/CDK2 activity begins in early S phase and increases during G 2. Cdc25B has been shown to dephosphorylate Tyr15 on CDK2 in early-to-mid G 2 in a manner similar to the aforementioned CDK1 mechanism. Downregulation of cyclin A2 in U2OS cells delays cyclin-B1/CDK1 activation by increasing Wee1 activity and lowering Plk1 and Cdc25C activity.
In some experiments, a researcher may want to control and synchronize the time when a group of cells progress to the next phase of the cell cycle. [5] The cells can be induced to arrest as they arrive (at different time points) at a certain phase, so that when the arrest is lifted (for instance, rescuing cell cycle progression by introducing another chemical) all the cells resume cell cycle ...