Einfluß von Coffein auf die Reparatur von UV-Prämutationen bei der phr⁻-Mutante von E. coli

Summary

The frequency of uv-induced S3-mutations (resistance to 3 γ Streptomycin/ml) in E. coli B/phr⁻/MC₂ was not significantly increased by postincubation in NB with caffeine, though an increase is to be expected if caffeine would inhibit the dark repair of the S3-premutations. The frequency was even decreased by high (≧0,1%) caffeine concentrations (Fig. 1), which indicates an enhancement of the (caffeine-resistant) repair. This enhancement may be caused indirectly by the observed prolongation by caffeine of the lag phase which gives more time for repair. Also the strong photoprotection and (indirect) photoreversion of the S3-mutations in this (non-photoreactivable) strain were not influenced by caffeine-posttreatment (Fig. 2 and 3). Thus, the dark repair assumed to be stimulated by pre- or post-illumination would be of the caffeine-resistant type. The repair of S3-premutations occurring during post-treatment in saline was inhibited by caffeine (Fig. 4). Also the dark-reactivation of cells killed by uv was inhibited by caffeine in the NB-agarmedium (Fig. 5). It is assumed that the repair of S3-premutations going on in NB-suspended cells is due to a mechanism which is not or only weakly inhibitable by caffeine and which is different from the caffeine-sensitive mechanism working under hunger conditions (perhaps by excising uv-products). Since reactivation of killed cells is caffeine-sensitive but reversion of S3-premutations is caffeine-resistant in NB-cells the uv-induced lethal lesions must be different from the S3-premutations.