Nucleotide excision repair (NER) is a DNA repair process employed to repair thymine dimers.
In NER, a UvrA dimer and UvrB bind to the DNA, recognising the thymine dimer structure, inducing a kink in the DNA strand. ATP hydrolysis causes the removal of the UvrA dimer, leaving UvrB bound to the thymine dimer site. UvrC is recruited, forming nicks either side of the dimer. A helicase (UvrD helicase II) enzyme removes the section of DNA containing the dimer between the nicks. UvrC and UvrB dissociate from the DNA, allowing DNA polymerase I and DNA ligase to fill the gap and seal the backbone.
Thymine dimers are mostly caused by UV damage to the DNA, causing two thymine bases next to each other to dimerise. This forms a disruption in the DNA strand, and is removed by this repair mechanism. Issues with the repair pathway can result in the formation of melanomas (skin cancers), which although rarely fatal, can metastasise.