What are two basic attributes of a cell cycle control system?

In Xenopus, one of the substrates of mitotic CDKs is the phosphatase Cdc25. When phosphorylated by mitotic CDKs, Cdc25 is activated. What is the substrate of Cdc25? How does this information help to explain the rapid rise in mitotic CDK activity as cells enter mitosis?

By what molecular pathway does loss of cell cycle regulation in an organism lead to cancer? What genetic changes can cooperate to accomplish the cancer cell’s escape from the normal balance of cell growth?

To identify genes controlling the cell cycle in budding yeast, a genetic screen was carried out. In this screen, haploid yeast cells were exposed to a DNA damaging agent to introduce random mutations in the genome. By culturing cells at an elevated temperature (e.g. 37 degrees), where many mutated genes lose their function, scientists identified yeast mutants that showed growth defects and arrest at specific stages of the cell cycle (e.g. in mitosis with large buds). In this screen, mutants of the cyclin-dependent kinase were identified, but not mutants of cyclins. Explain the reason for this outcome.

The Rb protein has been called the “master brake” of the cell cycle. Describe how the Rb protein acts as a cell cycle brake. How is the brake released in mid- to late G1 to allow the cell to proceed to S phase?

One approach to studying the regulation of cell cycle progression (particularly in an era when genetic and molecular biology manipulations were less readily accomplished in mammalian cells) was to use treatments that induced cells to fuse and then monitor the behavior of the two nuclei in the resulting cell. The figure below depicts data from one such study.  The investigators did preliminary work to produce populations of cells that were synchronized in various stages of the cell cycle (G1, S, or G2 in the examples shown below). They then fused the cells in different combinations and monitored subsequent events in each of the nuclei. For purposes of this question, we will pay particular attention to what occurred in the nucleus that came from the cell in G1. In one experiment (I), cells in the G1 and S phases were fused.  That event caused the nucleus from the G1 cell to very quickly enter the S phase (sooner than it would otherwise have done so).  In contrast, in a second experiment…

Explain Cyclin-dependent kinases (CDKs) control the cell cycle by phosphorylating other proteins?