Final answer:
A mutation in the DNA binding domain of p53 impedes its tumor-suppressing functions, allowing cells with damaged DNA to escape repair or apoptosis and continue dividing, resulting in tumor growth. Furthermore, it hampers the production of p21, leading to a compromised cell cycle checkpoint and a proliferation of mutations.
Step-by-step explanation:
A mutation in the DNA binding domain of p53 is a significant issue because p53 is a tumor suppressor protein that plays a critical role in preserving the integrity of the genome.
As a guardian of the cell cycle, particularly at the G₁ checkpoint, p53 ensures that cells with damaged DNA either repair the damage or undergo apoptosis (programmed cell death). However, when p53 is mutated, especially within its DNA binding domain, it becomes unable to perform its functions effectively.
Consequently, it may not detect errors in the DNA, fail to signal DNA repair enzymes, or be unable to trigger apoptosis. This allows cells with damaged DNA to continue dividing, propagating mutations and allowing the accumulation of further mutations.
Over time, this can lead to tumor growth as the cell cycle becomes unchecked due to the lack of functional p53's regulatory influence.
Additionally, mutated p53 can result in the loss of its ability to trigger the production of p21, a molecule that helps halt cell cycle progression.
This absence of p21 means there is no effective stop to Cdk activation, further compromising the G₁ checkpoint and allowing cells to progress to the S phase and divide under non-optimal conditions. This can lead to daughter cells with even more mutations, accelerating tumorigenesis.