Considering the sheer quantity of base pairs that need to be copied during replication, its amazing how accurate the cell can be. In addition, the assembly of the chromosomes via histones is incredible because of how much order there is to it and how much information they contain.
If cells were still able to replicate DNA, there would be too much DNA in the nucleus. This could lead to a number of issues with the cell, including cell death, or possibly even mutations if the overly copied DNA is able to make it into a fully formed cell. Perhaps this is a way that trisomy can occur.
This mechanism is crucial for the proper function of all cells in the body. If a cell was allowed to enter the M phase without having all of the nucleotides present, there would be missing genes. Therefore, certain proteins would be mutant or absent and the cell would not be able to function properly. This is the case for many genetic disorders and will almost always result in mutant cells.
Typically in a positive feedback loop the molecule that is upregulated is the one that results in the deactivation of the pathway. For example, in the hypothalamic pituitary axis, the hypothalamus stimulates the release of cortisol from the adrenal cortex, and the levels of cortisol dictate the amount of CRH released by the hypothalamus. CRH is the precursor in the pathway to the release of cortisol, and its levels are reduced when the levels of cortisol are high.
I did not realize that M-Cdk performed this function in the process of cellular replication. But, It makes a lot of sense. The phosphorylation of the lamin proteins must lead to a conformational shift that causes the depolymerization of the proteins and the degradation of the nuclear envelope. Its fascinating that the CDKs do so much of the work during M-phase.
I wonder if the delay is a result of the numerous kinases and pathway members required to activate the Cdc20-APC complex. If they are all in the cytosol or freely floating around, it will take time to transmit the signal. Also if there are a large number of members to the pathway, this could increase the amount of time to activate the complex. Furthermore, there could be a limiting reagent involved as the mechanism of delay.
This is a great example of a positive feedback loop. The Cdc20-APC complex is activated by the M-Cdks which are activated by the M-cyclins. Since the complex is activated by M-Cdks, the deactivation via ubiquitin-mediated proteolysis is done by the complex which then deactivates its activator. This must occur at a certain level of saturation or something like that because the M-cdks need to be active for a portion of the cell cycle.
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