Throughout the cell cycle there are a number of checkpoints which regulate cell progression from one phase to another. There is a G1 checkpoint that ensures everything is ready for DNA synthesis, a G2 checkpoint to determine whether the cell can proceed to M phase and a checkpoint within M phase to ensure the cell is ready to complete cell division.
Entry into each of the phases of the cell cycle are controlled by two classes of molecules, cyclins and cyclin dependent kinases (CDKs). Cyclins form the regulatory subunits and CDKs the catalytic subunits of an activated heterodimer; cyclins have no catalytic activity and CDKs are inactive in the absence of a partner cyclin. When activated by a bound cyclin, CDKs perform a biochemical reaction called phosphorylation that activates or inactivates target proteins to orchestrate coordinated entry into the next phase of the cell cycle. Different cyclin-CDK combinations determine which downstream proteins are targeted.
For example, during the latter stages of the G1 phase cyclin D1 forms a complex with CDK4, which subsequently phosphorylates and inactivates retinoblastoma (Rb) growth repression (Connell-Crowley et al, 1997). Conversely, growth arrest caused by DNA damage for example is the result of an up-regulation of CDK inhibitors such as p21 and p16 which bind to and inhibit the activity of CDK thereby preventing the phosphorylation of Rb (Aprelikova et al, 1995).
Figure 1: Basic overview of the eukaryotic cell cycle, showing each of the different phases