Describe the steps by which the \(p 53\) gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that \(p 53\) is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?

Answer: When DNA damage or cellular stress occurs, p53 is activated through phosphorylation by kinases like ATM and ATR. It then functions as a transcription factor, promoting cell-cycle arrest or apoptosis depending on the damage severity. Cell-cycle arrest allows for DNA repair, while apoptosis eliminates severely damaged cells. Individuals with one mutant copy of a recessive tumor-suppressor gene, like p53, are more likely to develop cancer because if they lose their remaining normal copy, the protective effect of the gene is lost. In contrast, individuals with two normal copies need to lose both copies for the tumor-suppressor function to be lost. This higher likelihood of losing the remaining normal copy puts carriers of a single mutant copy at a higher risk of developing cancer.