Proteins known as cyclins (named because their concentration increases and decreases in a regular pattern through the cell cycle) and enzymes known as cyclin-dependent kinases (Cdks) are the key components in the regulatory events that occur at checkpoints. At the G1 to S checkpoint, two different G1 cyclin/Cdk complexes form, resulting in activation of the kinases. The kinases catalyze a series of phosphorylations (addition of phosphate groups) of cell-cycle control proteins, affecting the functions of those proteins and leading to transition into the S phase.

A similar process occurs at the G2 to M checkpoint. A G2 cyclin binds to a Cdk to form a complex. Until the cell is ready to enter mitosis, phosphorylation of the CdK by another kinase keeps the Cdk inactive. At that time, a phosphatase removes the key phosphate from the Cdk, activating the enzyme. Phosphorylations of proteins by the Cdk move the cell into mitosis.

a. Why are genes encoding cyclins considered proto-oncogenes?

b. Why are mutations in cyclin genes (and in other proto-oncogenes) considered dominant mutations?