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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 ...
The degradation has an inhibitory effect on the formation of cyclin-dependent kinase complexes, which are key drivers of the cell cycle. [14] Through targeting Cdc25, cell cycle arrest can occur at multiple time points including the G1/S transition, S phase and G2/M transition. [8] Furthermore, Chk1 can target Cdc25 indirectly through ...
The cell cycle checkpoints play an important role in the control system by sensing defects that occur during essential processes such as DNA replication or chromosome segregation, and inducing a cell cycle arrest in response until the defects are repaired. [8]
Furthermore, to transition from cell cycle arrest to senescence, contact-inhibited cells must activate growth-activating pathways such as mTOR. [14] Once cells in high-density cultures become confluent enough such that the cell area falls below a critical value, [15] the adhesion formations trigger pathways that downregulate mitogen signaling ...
The enlarged cells that are able to re-enter the cell cycle are prone to DNA damage and experience abnormalities in signaling for repair (NHEJ pathway), eventually leading to a replication failure and a permanent cell-cycle exit. [24] Overall, a consistent correlation between larger cell size and senescence has been established.
Biochemical systems can also show hysteresis-like output when slowly varying states that are not directly monitored are involved, as in the case of the cell cycle arrest in yeast exposed to mating pheromone. Here, the duration of cell cycle arrest depends not only on the final level of input Fus3, but also on the previously achieved Fus3 levels.
For example, Cdk, or cyclin dependent kinase, is a major control switch for the cell cycle and it allows the cell to move from G1 to S or G2 to M by adding phosphate to protein substrates. Such multi-component (involving multiple inter-linked proteins) switches have been shown to generate decisive, robust (and potentially irreversible ...
[88] p53 prevents the cell from replicating by stopping the cell cycle at G1, or interphase, to give the cell time to repair; however, it will induce apoptosis if damage is extensive and repair efforts fail. [89] Any disruption to the regulation of the p53 or interferon genes will result in impaired apoptosis and the possible formation of tumors.