Discuss the events that may have contributed to the calculated time.
The length of the cell cycle is very variable.
In humans, cell turnover varies from a few hours in early embryonic development to an average of two to five days for epithelial cells, and to an entire human lifetime spent in G0 by specialized cells.
Each phase of the cell cycle has variations in the time that a cell spends.
The length of the cell cycle is about 24 hours when the cells are grown in a culture outside the body.
The cell cycle in fruit flies takes about eight minutes.
The time of the cell division cycle can be shortened by the fact that the nucleus of the fertilized egg does not go through cytokinesis until a multinucleate "zygote" is produced.
Both "invertebrates" and "vertebrates" have internal and external mechanisms that control the timing of events.
When the cell is about to begin the replication process, both the initiation and inhibition of cell division are triggered by external events.
Too much HGH can lead to gigantism, whereas a lack of it can lead to dwarfism.
Crowding of cells can affect cell division.
The size of the cell is a factor that can initiate cell division.
The solution is to divide.
A series of events within the cell allow the cell to proceed into interphase regardless of the source of the message.
Every cell cycle phase must be met or the cycle can't progress.
The daughter cells should be duplicate of the parent cells.
Every new cell produced from an abnormal cell may be passed on to other cells because of mistakes in the distribution of the chromosomes.
The checkpoints occur near the end of G1, at the G2/M transition and during metaphase.
Three checkpoints control the cell cycle.
The G1 checkpoint is where the integrity of the DNA is assessed.
There is a checkpoint called the G2 checkpoint.
The restriction point in yeast is called the G1 checkpoint and is where the cell irreversibly commits to the cell division process.
Growth factors play a large role in carrying the cell past the checkpoint.
There is a check for genomic DNA damage at the G1 checkpoint, as well as adequate reserves and cell size.
A cell that doesn't meet all the requirements won't be allowed to progress into the S phase.
The cell can either stop the cycle and try to remedy the problem, or it can advance into G0 and wait for the conditions to improve.
If certain conditions are not met, the G2 checkpoint bars entry.
At the G1 checkpoint, cell size and reserves are assessed.
Ensuring that all of the chromosomes have been replicated and that the replicated DNA is not damaged is the most important role of the G2 checkpoint.
The cell cycle is halted if the checkpoint mechanisms detect problems with the DNA.
The end of the metaphase stage of karyokinesis is near the M checkpoint.
The M checkpoint is used to determine if the sister chromatids are attached to the microtubules.
The cycle will not proceed until the kinetochores of each pair of sister chromatids are firmly anchored to the poles of the cell.
You can watch an animation of the cell cycle at the G1, G2, and M checkpoint by visiting this website.
There are two groups of molecules that regulate the cell cycle.
The regulatory molecule can either promote or stop the cell's cycle.
Regulator molecule can act individually, or they can influence the activity of other regulatory proteins.
If more than one mechanism controls the same event, the failure of a single regulator may have no effect on the cell cycle.
If multiple processes are affected, the effect of a deficient or non- functioning regulator can be fatal.
They are responsible for the progress of the cell.
The cell cycle has a predictable pattern for the levels of the four cyclin proteins.
External and internal signals can cause increases in the concentration of cyclin proteins.
Throughout the cell cycle, the concentrations of cyclin proteins change.
The three major cell-cycle checkpoint have a correlation with cyclin accumulation.
The decline of cyclin levels following each checkpoint is due to the degradation of cyclin by the cytoplasmic enzymes.
Cyclins only regulate the cell cycle when bound to Cdks.
The Cdk/cyclin complex must be phosphorylated in specific locations to be fully active.
Phosphorylation changes the shape of the protein.
The cell is advanced through the use of the proteins phosphorylated by Cdks.
The concentrations of cyclin fluctuate and determine when Cdk/cyclin complexes form.
Different cyclins and Cdks regulate different checkpoint in the cell cycle.
When fully activated, cyclin-dependent kinases can phosphorylate and thus help advance the cell cycle past a checkpoint.
To become fully activated, a Cdk must bind to a cyclin protein and be phosphorylated by another kinase.
The cell cycle is regulated by either the Cdk molecule alone or the Cdk/cyclin complexes because they are largely based on the timing of the cell cycle.
The cell cycle cannot proceed through the checkpoint without a specific concentration of fully activated cyclin/Cdk complexes.
The cyclins are the main regulatory molecule that determines the forward momentum of the cell cycle, but there are other mechanisms that fine- tune the cycle with negative, rather than positive, effects.
The progression of the cell cycle is blocked by these mechanisms.
There are Molecules that prevent the full activation of Cdks.
Many of these molecule directly or indirectly watch a cellcycle event.
The block placed on Cdks will not be removed until the specific event is completed.
Negative regulators stop the cell cycle.
In positive regulation, active molecules cause the cycle to progress.
Many cells have retinoblastoma proteins.
A dalton is equal to an atomic mass unit, which is 1 g/mol, and is referred to as the 53 and 21 designation.
Cell-cycle regulation comes from research conducted with cells that have lost control.
Cells that had begun to replicate uncontrollably were found to be damaged or non-functional with the three regulatory proteins.
The main cause of the progress through the cell cycle was a faulty copy.
p53 stops the cell cycle if it is found that the DNA is damaged.
p53 can cause cell suicide if the DNA can't be repaired.
The production of p21 is triggered when p53 levels rise.
It is less likely that the cell will move into the S phase if the levels of p53 and p21 accumulate.
Rb exerts its regulatory influence on other positive regulators.
In the active, dephosphorylated state, Rb bind to E2F.
Transcription factors allow the production of specific genes.
When Rb is bound to E2F, the production of the G1/S transition is blocked.
Rb becomes phosphorylated as the cell increases in size.
This particular block is removed after Rb releases E2F, which can turn on the gene that produces the transition protein.
Rb stops the cell cycle and lets it grow.
The cell cycle is negatively regulated by Rb and other proteins.