What is Excision repair?

Most lesions affect one strand and are repaired by cutting out the damaged piece and copying the other strand. Base excision repair (BER) handles small, non-distorting lesions: a DNA glycosylase specific for one kind of wrong base (uracil-DNA glycosylase, 8-oxoG glycosylase, and several others) flips the base out of the helix and cuts it off its sugar; an AP endonuclease nicks the backbone at the abasic site; a polymerase (Pol $\beta$) removes the sugar and inserts one nucleotide; a ligase seals. Nucleotide excision repair (NER) handles bulky, helix-distorting lesions — pyrimidine dimers, chemical adducts — without recognising the chemistry of the lesion itself: the distortion is detected (by XPC scanning the genome, or by a stalled RNA polymerase in the transcription-coupled branch), the helix is opened by the helicase subunits of TFIIH, the damage is verified (XPA), two endonucleases (XPF, XPG) cut the damaged strand $24\text{ to }32$ nucleotides apart, the oligonucleotide is released, and polymerase and ligase fill the gap. Loss of any of the seven XP proteins causes xeroderma pigmentosum: extreme sensitivity to sunlight, freckling, and a thousand-fold increased rate of skin cancer.