Non-homologous end joining

Definition

Non-homologous end joining (NHEJ) is a DNA repair mechanism that directly joins the broken ends of DNA together without the need for a homologous template. This process is essential for repairing double-strand breaks in DNA, which can occur due to various factors like radiation or chemical damage. NHEJ is a quick and efficient way to fix breaks, but it can lead to insertions or deletions, potentially causing mutations.

5 Must Know Facts For Your Next Test

1. NHEJ is the primary pathway for repairing double-strand breaks in mammalian cells and is active throughout the cell cycle.
2. The process begins with the recognition of broken DNA ends by the Ku protein complex, which then recruits additional proteins to facilitate end processing and ligation.
3. While NHEJ is generally efficient, it is error-prone and can result in mutations due to insertions or deletions at the repair site.
4. NHEJ can occur in both non-dividing and dividing cells, making it a crucial repair mechanism in various cellular contexts.
5. Deficiencies in NHEJ can lead to severe immunodeficiencies and increase susceptibility to cancer due to the accumulation of DNA damage.

Review Questions

• How does non-homologous end joining differ from homologous recombination in DNA repair?
  • Non-homologous end joining (NHEJ) differs from homologous recombination primarily in its repair mechanism and accuracy. NHEJ directly joins the broken ends of DNA without needing a template, making it a faster but less precise method. In contrast, homologous recombination uses a homologous sequence as a template to ensure accurate repair, thus reducing the risk of mutations. This fundamental difference highlights the trade-off between speed and fidelity in DNA repair processes.
• What role do Ku proteins play in the non-homologous end joining process?
  • Ku proteins play a crucial role in non-homologous end joining by binding to the ends of broken DNA strands. Once these proteins are attached, they help stabilize the broken ends and facilitate the recruitment of other proteins necessary for processing and ligation. This action is essential for effective repair, as Ku proteins serve as a bridge between the broken ends, ensuring they are aligned correctly for the subsequent joining process.
• Evaluate the implications of non-homologous end joining deficiencies on human health and disease.
  • Deficiencies in non-homologous end joining can have significant implications for human health, leading to conditions such as severe combined immunodeficiency (SCID) due to ineffective DNA repair in immune cells. These deficiencies can also contribute to an increased risk of cancer as unrepaired DNA breaks accumulate, resulting in genomic instability. The role of NHEJ in maintaining genome integrity underscores its importance not just in cellular function but also in preventing disease states related to improper DNA repair mechanisms.

Related terms

DNA double-strand break: A type of DNA damage where both strands of the DNA molecule are severed, leading to potential loss of genetic information.

homologous recombination: A more precise DNA repair mechanism that uses a homologous sequence as a template to accurately repair double-strand breaks.

Ku protein: A protein complex that plays a critical role in NHEJ by binding to the ends of broken DNA and facilitating their joining.