This mechanism can repair the damage caused by almost any large change in the structure of DNA double helix.
DNA lesion that cause large distortions in helical structure of DNA → repaired by NER
Suck "bulky lesions", include those created by covalent reaction of DNA bases with large hydrocarbons (such as carcinogen benzopyrene, found in tobacco smoke, coal tar and diesel exhaust), as well as pyrimidine dimers (T-T,T-C and C-C) caused by sunlight.
In humans NER, major defense against mutation caused by carcinogens- sunlight and tobacco smoke.
All cells have this elaborate pathway to correct pyrimidine dimers.
A large multienzyme complex scans the DNA for distortion in double helix, rather than specific base change.
Once it finds a lesion, it cleaves the phosphodiester backbone of the abnormal strand on both sides of the distortion.
DNA helicase peels away the single-strand olgionucleotide containing the lesion.
The large gap in DNA helix, repaired by DNA polymerase and DNA ligase.
NER: Steps
Uvr --> Ultraviolet light repair of pyrimidines
2 x UvrA and UvrB, scans the DNA and binds to the site of a lesion (e.g. pyrimidine dimer found!).
The UvrA dimer is then removed.
UvrC protein then binds to UvrB and cuts the damaged DNA strand at 2 sites (cuts phosphodiester bond, 8 nucleotdies away from the damaged site on 5' side and 4 nucleotides away on 3' side).
The 12 nucleotide fragment is then removed and separated (unwinds) from the DNA strand, by helicase (UvrD), the damaged region is then released.
DNA polymerase I enters the gap (formed by UvrD), to carry out repair synthesis. By joining complementary nucleotides in the 5' to 3' direction (on the gap).