Non-homologous end joining

Definition

Non-homologous end joining (NHEJ) is a crucial DNA repair mechanism that directly joins broken ends of double-stranded DNA without the need for a homologous template. This process is essential for maintaining genome stability, particularly in response to DNA damage caused by various environmental factors or cellular processes. NHEJ is often utilized in cells that are in the G1 phase of the cell cycle when homologous recombination is not available.

5 Must Know Facts For Your Next Test

1. NHEJ is the primary pathway for repairing double-strand breaks in mammalian cells and is especially important in non-dividing cells.
2. The process involves the recognition of broken DNA ends, followed by end processing and ligation to rejoin the strands.
3. NHEJ can lead to small insertions or deletions at the repair site, which can result in mutations that may affect gene function.
4. This repair mechanism is generally quicker than homologous recombination but is less accurate, making it more prone to errors.
5. NHEJ is active throughout the cell cycle but is predominantly used in the G1 phase when sister chromatids are not available for homologous recombination.

Review Questions

• How does non-homologous end joining differ from homologous recombination in terms of mechanisms and outcomes?
  • Non-homologous end joining (NHEJ) differs from homologous recombination primarily in its mechanism of action and accuracy. NHEJ directly ligates broken DNA ends without a template, making it a faster process but more prone to errors, potentially resulting in mutations. In contrast, homologous recombination uses a homologous DNA sequence as a template for precise repair, which generally leads to fewer mutations but takes longer and is only available during certain phases of the cell cycle.
• Discuss the role of Ku protein in the non-homologous end joining process and its importance in cellular responses to DNA damage.
  • Ku protein plays a vital role in the non-homologous end joining process by recognizing and binding to the free ends of broken DNA. Once bound, Ku stabilizes the ends and recruits additional proteins necessary for processing and ligation. This makes Ku essential for ensuring efficient and accurate repair of DNA double-strand breaks, allowing cells to respond quickly to damage and maintain genomic integrity.
• Evaluate the implications of non-homologous end joining's error-prone nature on cancer development and treatment strategies.
  • The error-prone nature of non-homologous end joining has significant implications for cancer development since it can introduce mutations that lead to oncogene activation or tumor suppressor gene inactivation. This raises concerns about how NHEJ affects genomic stability over time. In terms of treatment strategies, targeting NHEJ could be a potential approach in cancer therapies, particularly for tumors that exhibit high levels of reliance on this repair pathway. Understanding how to manipulate NHEJ could improve treatment outcomes by increasing the effectiveness of therapies that induce DNA damage in cancer cells.

Related terms

DNA Double-Strand Breaks: Severe forms of DNA damage where both strands of the DNA helix are broken, which can lead to cell death or cancer if not properly repaired.

Homologous Recombination: A more precise DNA repair mechanism that uses a homologous sequence as a template for accurate repair of double-strand breaks.

Ku Protein: A protein that plays a critical role in the recognition and binding of broken DNA ends during the non-homologous end joining process.