Nucleotide excision repair (NER) is a multi-enzyme excision repair pathway targetted at damaged segments of DNA. A nucleotide with abnormal alterations in its chemical properties is termed an elementary damage site (EDS). UV light is a frequent cause of damage to segments of DNA.
Similar mechanisms for NER exist in both prokaryotes and eukaryotes, and the mechanism is highly conserved in eukaryotes. The recognition of DNA damage is less specific in nucleotide excision repair (NER) than in base excision repair (BER), which targets damaged bases. Thus NER repairs a wider range of damage types than BER, irrespective of chromatin structure or the gene expression profile of a particular cell.
NER operates by: (a) recognition of the damaged DNA; (b) excision of an oligonucleotide of 24–32 residues by dual incision of the damaged strand on each side of the lesion; and, as for BER (c) filling in of the resulting gap by DNA polymerase; and (d) ligation of the nick. There is evidence that at least some steps of NER require ATP-dependent chromatin remodeling activities.
NER can operate by two pathways. The first pathway, global genome repair (GGR), acts on DNA lesions across the genome and is transcription-independent. The second NER pathway, transcription coupled repair, is coupled to active transcription and is directed to the transcribed strand of active genes. clickable diagram - nucleotide excision repair : diagram>nucleotide excision repair : diagram>transition coupled repair : more detail NER defective medical disorders : free full text review article :
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