In March 2011 an earthquake measuring approximately 9.0 on the Richter scale struck Fukushima, Japan. Several nuclear reactors at the Fukushima Daichii Nuclear Power Plant were damaged, and nuclear core meltdown occurred. A massive release of radiation accompanied damage to the plant, and 5 years later the incidence of thyroid cancer in children exposed to the radiation was determined to be well over 100 times more frequent than expected without radiation exposure. DNA damage and mutations resulting from radiation exposure are suspected of causing this increased cancer rate. What gene discussed in this chapter might be responsible for pausing the cell cycle of dividing cells long enough for radiation-induced damage to be repaired in cells?

Verified step by step guidance

1. Identify the context of the problem: The question is asking about a gene that plays a role in pausing the cell cycle to allow for DNA repair after radiation-induced damage. This is a key concept in genetics related to cell cycle regulation and DNA damage response.
2. Recall the function of tumor suppressor genes: Tumor suppressor genes are responsible for preventing uncontrolled cell division and ensuring that damaged DNA is repaired before the cell continues to divide. One such gene is central to this process.
3. Focus on the p53 gene: The p53 gene is a well-known tumor suppressor gene that plays a critical role in responding to DNA damage. It can pause the cell cycle at the G1/S checkpoint, allowing time for DNA repair mechanisms to fix the damage.
4. Understand the mechanism: When DNA damage is detected, p53 is activated and leads to the production of proteins like p21. These proteins inhibit cyclin-dependent kinases (CDKs), which are necessary for the cell to progress through the cell cycle. This pause allows the cell to repair its DNA or, if the damage is too severe, to undergo apoptosis (programmed cell death).
5. Connect the gene to the problem: In the context of radiation exposure, such as the Fukushima incident, the p53 gene would be crucial in pausing the cell cycle to repair radiation-induced DNA damage. If p53 is mutated or non-functional, cells may continue to divide with damaged DNA, increasing the risk of cancer, such as thyroid cancer in this case.

Key Concepts

Cell Cycle Regulation

The cell cycle is a series of phases that a cell goes through to divide and replicate. Regulation of this cycle is crucial for maintaining genomic integrity, especially in response to DNA damage. Key proteins, such as cyclins and cyclin-dependent kinases (CDKs), control the progression through the cycle, while checkpoints ensure that damaged DNA is repaired before the cell continues to divide.

DNA Damage Response (DDR)

The DNA Damage Response is a network of cellular pathways that detect and repair DNA damage. When cells experience stress, such as radiation exposure, DDR mechanisms activate to halt the cell cycle, allowing time for repair processes to occur. Key proteins involved in this response include p53, which can induce cell cycle arrest, apoptosis, or DNA repair, depending on the extent of the damage.

p53 Tumor Suppressor Gene

The p53 gene encodes a protein that plays a critical role in regulating the cell cycle and maintaining genomic stability. Often referred to as the 'guardian of the genome,' p53 is activated in response to DNA damage and can induce cell cycle arrest, allowing for repair mechanisms to function. Mutations in the p53 gene are commonly associated with various cancers, highlighting its importance in preventing tumorigenesis.