base excision repair
/ BER /
Base excision repair is the cell's small-scale handyman, specialised for fixing single damaged or wrong bases — the kind of everyday chemical wear that does not bend the helix much. Think of a book with a few letters smudged or faded: you don't reprint the page, you erase the bad letter and pencil in the right one. That is exactly the spirit of base excision repair.
It runs in clean steps. A specialised enzyme called a DNA glycosylase patrols the DNA and recognises one specific kind of damaged or inappropriate base — a uracil that arose from deaminated cytosine, an oxidised base, an alkylated base. The glycosylase flips that base out and snips it free from the sugar, leaving an empty abasic site. A second enzyme nicks the backbone there; a repair polymerase fills the single-nucleotide gap by reading the intact opposite strand; and DNA ligase seals the nick. The damaged letter is gone, the correct one is in its place, and the backbone is whole again.
Base excision repair is the front line against the relentless spontaneous and oxidative damage that batters DNA every day, especially the constant deamination of cytosine and the oxidation of guanine. Because each glycosylase is tuned to one type of lesion, the cell carries a whole toolkit of them. The pathway is so fundamental that its breakdown raises mutation rates and cancer risk, and it neatly complements the bulkier-lesion pathway, nucleotide excision repair, dividing the repair workload by the size and shape of the damage.
Uracil DNA glycosylase finds a uracil (from a deaminated cytosine), flips it out, and cuts it from the backbone. A polymerase then re-inserts the correct cytosine using the opposite strand, and ligase seals up.
One bad base out, one correct base in — a single-letter edit guided by the intact strand.
Base excision repair handles small, non-helix-distorting damage one base at a time; bulky lesions that kink the helix, like UV dimers, are the job of nucleotide excision repair instead.