Cell cycle checkpoints

Definition

Cell cycle checkpoints are regulatory mechanisms in the cell cycle that ensure the proper progression of cell division. These checkpoints monitor the integrity of DNA, the completion of DNA replication, and the alignment of chromosomes during mitosis, allowing for errors to be detected and corrected before moving on to the next phase. The disruption of these checkpoints can lead to uncontrolled cell growth, which is often exploited by viral oncoproteins to promote cancer development.

5 Must Know Facts For Your Next Test

1. There are three major checkpoints in the cell cycle: the G1 checkpoint, the G2 checkpoint, and the M checkpoint, each serving to ensure that specific conditions are met before progression.
2. At the G1 checkpoint, the cell assesses its size, nutrient availability, and DNA integrity before committing to DNA synthesis.
3. The G2 checkpoint ensures that DNA replication has been completed accurately and that any damage is repaired before the cell enters mitosis.
4. The M checkpoint occurs during metaphase of mitosis and verifies that all chromosomes are properly attached to the spindle apparatus before allowing anaphase to proceed.
5. Viral oncoproteins can interfere with these checkpoints by inactivating tumor suppressor proteins like p53 or retinoblastoma protein (Rb), leading to unregulated cell division.

Review Questions

• How do cell cycle checkpoints function to maintain genomic integrity during cell division?
  • Cell cycle checkpoints function as surveillance mechanisms that assess various conditions within the cell before allowing progression to the next phase. For example, the G1 checkpoint evaluates DNA integrity and environmental conditions, while the G2 checkpoint checks for proper DNA replication. If any issues are detected, such as DNA damage or incomplete replication, the checkpoints can halt the cycle to allow for repair or trigger apoptosis if necessary, thereby maintaining genomic integrity.
• Discuss how viral oncoproteins can manipulate cell cycle checkpoints to promote oncogenesis.
  • Viral oncoproteins can manipulate cell cycle checkpoints by targeting key regulatory proteins that control these checkpoints. For instance, some viruses produce proteins that bind to and inactivate tumor suppressor proteins like p53 and Rb. This inactivation allows cells to bypass critical checkpoints, leading to unregulated cell division and increased risk of tumor formation. By overriding these cellular safeguards, viruses can drive their own replication and contribute to oncogenesis.
• Evaluate the implications of disrupted cell cycle checkpoints in cancer therapy and viral infections.
  • Disrupted cell cycle checkpoints have significant implications for both cancer therapy and viral infections. In cancer therapy, understanding how tumors exploit checkpoint deficiencies can lead to targeted treatments that restore normal checkpoint function or enhance apoptosis in cancer cells. Conversely, in viral infections, knowing how viruses manipulate these checkpoints opens avenues for developing antiviral therapies that could inhibit viral replication by reinstating proper checkpoint controls. Ultimately, studying these interactions reveals critical insights into both cancer biology and virology.

Related terms

Tumor suppressor genes: Genes that help regulate cell division and prevent tumor formation by encoding proteins that can halt the cell cycle in response to DNA damage.

Oncogenes: Mutated forms of normal genes (proto-oncogenes) that, when activated, contribute to cancer development by promoting excessive cell proliferation.

Apoptosis: The process of programmed cell death that eliminates damaged or unwanted cells, playing a critical role in maintaining cellular homeostasis.