Note: This section goes into greater detail than is necessary for classes on the level of AP Biology. It does, however, provide further insight into the processes behind cell regulations that AP Biology glosses over.
In this section, we will review the biological regulators of the cell cycle. Control of the cell cycle is necessary for a couple of reasons. First, if the cell cycle were not regulated, cells could constantly undergo cell division. While this may be beneficial to certain cells, on the whole constant reproduction without cause would be biologically wasteful. Second, internal regulation of the cell cycle is necessary to signal passage from one phase to the next at appropriate times. This regulation is not achieved through strict time constraints, but rather with feedback from the cell.
We already discussed some regulatory issues when we talked about cellular conditions necessary for passage from G1 and G2. Here, we will discuss more specifically the proteins that interact to regulate the cell cycle. The "checkpoints" that we described earlier are established by proteins that use cues from the cell's environment to trigger the entry to and exit from the distinct phases of the cell cycle. We will discuss two main families of proteins involved in this process—cyclin-dependent protein kinases (Cdks) and cyclins.
A Cdks is an enzyme that adds negatively charged phosphate groups to other molecules in a process called phosphorylation. Through phosphorylation, Cdks signal the cell that it is ready to pass into the next stage of the cell cycle. As their name suggests, Cyclin-Dependent Protein Kinases are dependent on cyclins, another class of regulatory proteins. Cyclins bind to Cdks, activating the Cdks to phosphorylate other molecules.
Cyclins are named such because they undergo a constant cycle of synthesis and degradation during cell division. When cyclins are synthesized, they act as an activating protein and bind to Cdks forming a cyclin-Cdk complex. This complex then acts as a signal to the cell to pass to the next cell cycle phase. Eventually, the cyclin degrades, deactivating the Cdk, thus signaling exit from a particular phase. There are two classes of cyclins: mitotic cyclins and G1 cyclins.
G1 cyclins bind to Cdk proteins during G1. Once bound and activated, the Cdk signals the cell's exit from G1 and entry into S phase. When the cell reaches an appropriate size and the cellular environment is correct for DNA replication, the cyclins begin to degrade. G1 cyclin degradation deactivates the Cdk and leads to entry into S phase.
Mitotic cyclins accumulate gradually during G2. Once they reach a high enough concentration, they can bind to Cdks. When mitotic cyclins bind to Cdks in G2, the resulting complex is known as Mitosis-promoting factor (MPF). This complex acts as the signal for the G2 cell to enter mitosis. Once the mitotic cyclin degrades, MPF is inactivated and the cell exits mitosis by dividing and re- entering G1. The cellular signals that we described earlier (cell size, completion of DNA replication, and cellular environment) provide the signals that regulate the synthesis and degradation of cyclins.