dubbelstrengsbreuk

Dubbelstrengsbreuk, also known as double-strand break (DSB), refers to a type of DNA damage where both strands of the DNA double helix are severed simultaneously. This form of DNA damage can occur due to various factors, including ionizing radiation, certain chemicals, or cellular processes such as replication stress. Because the integrity of the genetic information is compromised, dubbelstrengsbreuk poses a significant threat to cell survival and genetic stability.

The repair of dubbelstrengsbreuk is critical for maintaining genomic integrity and is primarily achieved through two central pathways: homologous recombination (HR) and non-homologous end joining (NHEJ). Homologous recombination uses a homologous sequence as a template to accurately repair the break, often during the S and G2 phases of the cell cycle when sister chromatids are available. Non-homologous end joining, on the other hand, directly ligates the broken DNA ends without the need for a template, which can sometimes lead to mutations.

Cells have evolved sophisticated mechanisms to detect and respond to DSBs, including signaling pathways that activate repair proteins and cell cycle checkpoints to prevent the propagation of damaged DNA. Failure to efficiently repair dubbelstrengsbreuk can result in mutations, chromosomal rearrangements, or cell death, and is implicated in aging, cancer, and other genetic disorders.

Understanding the mechanisms behind dubbelstrengsbreuk and its repair processes is vital in areas such as cancer research and radiobiology, where DNA damage and repair influence treatment outcomes. Advances in this field continue to inform the development of targeted therapies and protective strategies against genotoxic stress.