Final answer:
Proteins like cyclins and Cdks regulate the cell cycle and are marked for degradation by proteasomes once their role is complete to ensure proper cell progression. p53 and p21 are involved in the G1 checkpoint, halting the cell cycle in response to DNA damage and can lead to apoptosis if repair is not possible.
Step-by-step explanation:
The destruction of certain proteins during the cell cycle is a key regulatory mechanism to ensure cells progress properly through the cell cycle checkpoints. Proteins such as cyclins and cyclin-dependent kinases (Cdks) are central to this process. As the cell moves through the cycle, levels of cyclins increase, forming active complexes with Cdks which are necessary to push the cell into the next phase. Once the cell progresses, these cyclins are marked for degradation by proteasomes to prevent inappropriate reactivation of the checkpoints. Similarly, proteins like p53 and p21 act at the G1 checkpoint to prevent the division of cells with damaged DNA by either repairing the DNA or inducing apoptosis, and also are regulated by changes in their levels and activities.
Proteasomes target protein complexes such as the Chk2-cyclin complex for degradation when they are no longer needed, thus preventing their accumulation and potential interference with the cell cycle's ordered progression. Additionally, elevated levels of p53 lead to increased production of p21, which in turn inhibits Cdk/cyclin complexes, reinforcing the cell's halt at the G1 checkpoint in the face of DNA damage or stress. This elegant system of protein regulation aids in maintaining the healthy function of cellular division and in preventing the proliferation of potentially cancerous cells.