תיקון על ידי קטיעת נוקלאוטידים

Nucleotide excision repair, or NER, fixes bulky DNA lesions caused by UV radiation and chemical carcinogens.

These bulky lesions, such as pyrimidine dimers, distort the DNA helix and interfere with DNA replication and transcription.

In E. coli, the repair proteins UvrA  and UvrB form a complex that scans the genomic DNA for structural lesions.

Once it encounters a lesion, the UvrA dissociates, causing UvrB to bind tightly to the distorted DNA.

The DNA-bound UvrB then recruits UvrC, an endonuclease, which makes an incision on either side of the lesion.

Next, the UvrD  helicase unwinds the DNA and excises the fragment carrying the lesion.

Following excision, DNA polymerase fills the gap with new complementary nucleotides, and the enzyme DNA ligase seals the gap between the new and old DNA, completing the repair.

Alternately, if an actively transcribing RNA polymerase encounters the bulky lesion, it can directly recruit the UvrB to the site of the lesion.

This initiates transcription-coupled nucleotide excision repair that proceeds in the same manner as regular NER to complete the repair and continue transcription.