Question

Which of these is not true of the gene \(p 53 ?\) a. Mutations of both proto-oncogenes and tumor-suppressor genes lead to inactivity of \(p 53\) b. Normally, \(p 53\) functions to stop the cell cycle and initiate repair enzymes, when necessary. c. Normally, \(p 53\) restores the length of telomeres. d. Cancer cells shut down the activity of \(p 53\), even though it may be present.

Short answer

The statement that is not true about gene p53 is option c: Normally, \(p 53\) restores the length of telomeres.

Step-by-step solution

Statement a. Mutations of both proto-oncogenes and tumor-suppressor genes lead to inactivity of \(p 53\)

Statement a is True: Mutations in proto-oncogenes and tumor-suppressor genes can indeed render p53 inactive. This inactivity can lead to uncontrolled cell growth and eventually cancer.

Statement b. Normally, \(p 53\) functions to stop the cell cycle and initiate repair enzymes, when necessary.

Statement b is True: p53 is a tumor suppressor gene that helps control the cell cycle, allowing cells to repair any damage before they divide. When DNA damage is detected, p53 will stop the cell cycle and initiate the process of DNA repair.

Statement c. Normally, \(p 53\) restores the length of telomeres.

Statement c is False: p53 does not play a role in restoring telomere lengths. Its main function is to control the cell cycle and initiate DNA repair when necessary. Telomere maintenance is mainly carried out by an enzyme called telomerase.

Statement d. Cancer cells shut down the activity of \(p 53\), even though it may be present.

Statement d is True: In many types of cancer, the function of p53 is often disrupted or shut down. This allows the cancer cells to escape the cell cycle control mechanisms and continue to multiply uncontrollably. Thus, the statement that is not true about gene p53 is option c. Normally, \(p 53\) restores the length of telomeres.

Key concepts

Tumor-Suppressor Genes

Tumor-suppressor genes are like the body's own crime scene investigators, always on the lookout for any DNA damage that could lead to cancer. The p53 gene is one of the most important of these guardians. Its job is to keep cells from growing out of control by ordering damaged cells to either repair themselves or bow out gracefully through a process called apoptosis.

The p53 acts like a strict quality control inspector in a factory, halting the production line (the cell cycle) when it finds a problem. If damage is found, p53 can activate other genes to fix the errors or send the irreparable cells off to be recycled. It's such an important part of our cells' anti-cancer defense that when p53 itself is mutated, the results can be disastrous, leading to tumor growth because the cells lose their ability to regulate themselves or to commit suicide when they become a danger.

Cell Cycle Regulation

If we think of the cell cycle as a set of traffic lights controlling the flow of traffic through a city, the p53 gene is the traffic cop making sure everyone obeys the signals. It's responsible for stopping the cell cycle dead in its tracks at a checkpoint if there's any sign of trouble, like DNA damage.

p53 looks out for abnormalities and, when it detects something wrong, it slams on the brakes, stopping the cycle at one of two checkpoints. These checkpoints act as quality assurance stages, where cells are thoroughly inspected for DNA damage before being allowed to proceed to replicate (the G1/S checkpoint) or divide (the G2/M checkpoint). If p53 is inactivated due to a mutation, it's like having a traffic cop sleeping on the job—cells can proceed unchecked and can accumulate errors leading to cancer development.

DNA Repair

Much like a maintenance crew that's always on call to patch up potholes or fix broken streetlights in a city, the p53 gene helps to coordinate the repair of DNA damage in our cells. If p53 finds genetic damage, it doesn't just stop the cell cycle; it also sounds the alarm to call in the repair crew.

p53 can activate a whole bunch of different genes that send in proteins to repair the DNA, stitch it back together, and make sure the genetic information is correct. Sometimes, though, the damage to the DNA is beyond repair. In those cases, p53's role is to prevent the cell from becoming a hazard. Rather than letting the cell divide and potentially lead to cancer, p53 commands the cell to self-destruct. Even though one might think this could play a role in telomere maintenance, p53 actually does not directly restore telomere length. Instead, it maintains genomic integrity by focusing on repairing mutations and lesions that occur throughout our DNA.