Question 1: The Role of Gap Phases in Cell Cycle Regulation
If the main function of the cell cycle is to regulate the duplication of DNA in S-phase and the distribution of duplicated chromosomes in M-phase, why are there gaps between S-phase and M-phase? What are the functions of those gaps? Why are they important for cell division?
Question 2: The Regulation of CDK Activity
What are ways in which CDK is regulated during the cell cycle?
Question 3: Checkpoints
RNR1 is a gene that makes the ribonucleotide reductase protein required to synthesize nucleotides for DNA replication. Hydroxyurea (HU) is a molecule that inhibits the function of this enzyme. If you were to add HU to your cells, in which phase of the cell cycle do you think that cells would pause?
Question 4: Checkpoints
Nocodazole is drug that causes microtubules to depolymerize. This drug is used to halt the cells in a particular phase of the cell cycle. Which checkpoint would you expect was activated?
Question 5: p53 Regulation of the Cell Cycle
p53 is constitutively degraded when not active. What would be the result if p53 were degraded even when active (say a gain of function mutation in the ubiquitin ligase that targets p53)? Would this cause an increased or decreased response to DNA damage and would this lead to a cancerous phenotype or to more programmed cell death?
Question 6: DNA Damage Effect on Cell Cycle Regulation
You spend too much time in the sun and get sunburned, which means that the cells in your skin have been exposed to a high amount of UV irradiation leading to DNA damage. What would you expect to be occurring in your cells after they've experienced this DNA damage due to UV irradiation? For each of the following explain yes or no, why or why not...
1. Rb is phosphorylated
2. E2F is inactive
3. CDK inhibitors are active
4. p53 is bound to DNA
Question 7: Role of Cyclin-Dependent Kinases in Controlling the Cell Cycle
Based on your understanding of the regulation of the eukaryotic cell cycle, how could you explain the experimental observation that when purified S-cyclin/CDK protein complex is injected into cells that have just finished dividing and are entering G1-phase, preRCs do not form on origins of replication and the cells never enter S-phase?
Question 8: The Role of CDK in DNA Replication
It has been shown experimentally that CDK is required for DNA replication, however it does not directly trigger origin firing. What role does CDK play in DNA replication? What wouldn't happen during the process of getting set up for DNA replication if CDK activity were inhibited?