In nucleotide excision repair (NER), damaged bases are cut out within a string of nucleotides, and replaced with DNA as directed by the undamaged template strand. This repair system is used to remove pyrimidine dimers formed by UV radiation as well as nucleotides modified by bulky chemical adducts.
The common feature of damage that is repaired by nucleotide excision is that the modified nucleotides cause a significant distortion in the DNA helix. NER occurs in almost all organisms examined. Some of the best-characterized enzymes catalyzing this process are the UvrABC excinuclease and the UvrD helicase in E. coli. The genes encoding this repair function were discovered as mutants that are highly sensitive to UV damage, indicating that the mutants are defective in UV repair.
Wild type E. coli cells are killed only at higher doses of UV radiation. Mutant strains can be identified that are substantially more sensitive to UV radiation; these are defective in the functions needed for UV-resistance, abbreviated uvr. By collecting large numbers of such mutants and testing them for their ability to restore resistance to UV radiation in combination, complementation groups were identified.
Four of the complementation groups, or genes, encode proteins that play major rules in NER; they are uvrA, uvrB, uvrC and uvrD.
See Video: Nucleotide Excision Repair of DNA.
Video Source: All About Molecular Biology
