double strand dna repair
17 18 particular pathways of both homologous recombination repair and non homologous end joining rely on ercc1 xpf function. Dna repair is a collection of processes by which a cell identifies and corrects damage to the dna molecules that encode its genome. Homologous recombination hr and nonhomologous dna end joining nhej.
In 1953 the race to determine how these pieces fit together in a three dimensional structure was won by james watson and francis crick at the cavendish laboratory in cambridge england.

Double strand dna repair. The various causes of double strand breaks dsbs result in a diverse chemistry of dna ends that must be repair. Defects in nh. Indeed a protein complex containing a dna endonuclease and or exonuclease seems to be involved in dna double strand break repair. X ray crystallography provided the final clue that the dna molecule is a double helix shaped like a twisted ladder.
Dna double strand breaks dsbs interrupting the genetic information are elicited by various environmental and endogenous factors. Dna repair to resolve the heteroduplex by copying the information in the edited strand to the complementary strand would permanently install the edit fig. They bear the risk of cell lethality and if mis repaired of deleterious mutation. Dna double strand breaks dsbs are the most dangerous type of dna damage because they can result in the loss of large chromosomal regions.
In all mammalian cells dsbs that occur throughout the cell cycle are repaired predominantly by the non homologous dna end joining nhej pathway. Most dna double strand breaks are not blunt ended but have single stranded overhangs. Double strand dna breaks are common events in eukaryotic cells and there are two major pathways for repairing them. However if deployed in an inappropriate cellular context these same repair functions can.
This biological process consists of end resection strand invasion and subsequent dna synthesis and resolution of holliday junctions. In human cells both normal metabolic activities and environmental factors such as radiation can cause dna damage resulting in tens of thousands of individual molecular lesions per cell per day. The major pathways of dna double strand break dsb repair are crucial for maintaining genomic stability. Many of these lesions cause structural damage to the dna molecule.
These dna ends might need to be trimmed by exonucleases and or endonucleases before they can be rejoined.





























































































