Abstract
Abstract— In stationary‐phase Escherichia coli B/r, photoreactivation (PR) at 313 nm of ultraviolet (u.v.) killing is inefficient compared with PR at 405 nm, and can be explained solely by photoenzymatic reversal of pyrimidine dimers.In Staphylococcus epidermidis, PR shows a maximum at 313 nm, suggesting that this organism shows the Type III PR proposed by Jagger et al.[5] for Streptomyces strains. Reversal of pyrimidine dimers is not sufficient to explain this PR. The mechanism of Type III PR remains unknown.With both S. epidermidis and E. coli B/r, the amount of uracil–thymine heteroadduct in DNA hydrolysates decreases if the cells are given a post‐u.v. treatment at 313 nm, but no decrease is observed if the post‐u.v. treatment is at 405 nm. The biological significance of this adduct and of its removal is not clear. It may play a role in Type III PR.
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