Two mechanisms of DNA repair that bacteria can use are photoreactive repair or UV repair.
UV-induced pyrimidine dimers can be directly repaired by photoreactive repair, a DNA repair mechanism found in bacteria, single-celled eukaryotes, plants, and some animals (e.g., Drosophila), but not in humans. Photoreactivation uses
photolyase to break the bonds formed during pyrimidine dimerization.
UV-induced damage to DNA can also be fixed by UV repair, which involves excision of a short region of the strand containing the photoproduct, followed by synthesis of new DNA to replace the excised region. In E. coli, the UVR-BC complex cleaves a pair of
phosphodiester bonds on the strand containing the photoproduct, releasing a 12-bp fragment of DNA surrounding the mutation. UVR-D, a helicase, binds along with DNA pol I, allowing the polymerase to use the complementary strand to synthesize a replacement for the missing segment.
DNA ligase then binds to the region to seal the sugar-phosphate backbone.
Photoreactive repair requires light to power the repair mechanism, so placing the bacteria in dark after the damage has occurred would mean fewer repairs would take place. Also, there would be a decrease in bacteria viability in the dark as compared to the light.