Final answer:
Rb, p53, and p21 promote cell cycle arrest by halting the cell cycle in response to damaged DNA and stress. p53 recruits enzymes to repair the DNA or induces apoptosis if repair is not possible. p21 inhibits Cdk/cyclin complexes, enforcing the cell cycle arrest dictated by p53. Rb blocks the cell cycle by binding to transcription factors, releasing its hold when phosphorylated and allowing gene expression for cell cycle progression.
Step-by-step explanation:
Rb, p53, and p21 act primarily at the G₁ checkpoint. When damaged DNA is detected during the preparatory processes in G₁ phase, p53 halts the cell cycle and recruits enzymes to repair the DNA. If the DNA cannot be repaired, p53 can induce apoptosis to prevent the duplication of damaged chromosomes. As p53 levels rise, it triggers the production of p21, which binds to and inhibits the activity of the Cdk/cyclin complexes, enforcing the cell cycle arrest dictated by p53. Higher levels of p53 and p21 accumulate under stress, making it less likely for the cell to move into the S phase.
Rb exerts its regulatory influence on other positive regulator proteins. In its active state, Rb binds to transcription factors like E2F, blocking the production of proteins necessary for the G1/S transition. As the cell increases in size, Rb is gradually phosphorylated and becomes inactivated, releasing E2F and allowing gene expression for the transition protein, thus advancing the cell cycle. Rb is a tumor suppressor because it inhibits cell division when not phosphorylated.