Nucleotide excision repair
Nucleotide excision repair (NER) is a DNA repair mechanism that is essential for maintaining the integrity of the genome. It is a versatile system that can recognize and repair a wide range of structurally unrelated DNA damage, including ultraviolet (UV) light-induced pyrimidine dimers and chemical carcinogen-induced bulky adducts.
Mechanism[edit | edit source]
NER operates through a cut-and-patch mechanism. It involves the following steps:
- Damage recognition: The first step in NER is the recognition of DNA damage. This is achieved by a complex of proteins, including XPC (xeroderma pigmentosum complementation group C) and HR23B (RAD23 homolog B).
- Excision: Once the damage is recognized, the DNA around the damage site is unwound and a single-stranded DNA segment containing the lesion is excised. This is carried out by the endonucleases XPF (xeroderma pigmentosum complementation group F) and ERCC1 (excision repair cross-complementation group 1).
- Repair synthesis: The gap left by the excision is filled in by a DNA polymerase, which synthesizes new DNA using the undamaged strand as a template.
- Ligation: Finally, the newly synthesized DNA is joined to the existing DNA by a DNA ligase.
Clinical significance[edit | edit source]
Defects in NER can lead to several human disorders, such as xeroderma pigmentosum (XP), Cockayne syndrome (CS), and trichothiodystrophy (TTD). These disorders are characterized by sensitivity to UV light and a predisposition to skin cancer.
NER is also a target for cancer therapy. Many chemotherapeutic drugs work by inducing DNA damage that is recognized and repaired by NER. Inhibiting NER can therefore enhance the effectiveness of these drugs.
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Credits:Most images are courtesy of Wikimedia commons, and templates Wikipedia, licensed under CC BY SA or similar.Contributors: Prab R. Tumpati, MD