Effect of protein synthesis inhibition on recovery of UV- and gamma-irridated Schizosaccharomyces pombe from repair inhibition by caffeine.
The progress of repair in Schizosaccharomyces pombe may be followed during post-irradiation incubation by measuring, after various intervals, the ability of UV- or gamma-irradiated cells to avoid enhanced lethality when exposed to the repair inhibitor caffeine (Gentner and Werner, 1975). This technique has now been used to investigate the effect of inhibition of protein synthesis on repair of UV- and gamma-irradiation-induced damage in this organism. When protein synthesis was inhibited with cycloheximide in UV-irradiated wild-type cells, only a small amount of recovery from caffeine inhibition occurred; this indicated that post-irradiation protein synthesis was required for repair, and in particular for the recombinational repair pathway, which is a major mechanism for repair of UV damage in this organism. In gamma-irradiated wild-type cells, inhibition of post-irradiation protein synthesis reduced the rate of recovery from repair inhibition by caffeine, but full recovery from caffeine-sensitive damage did occur at longer incubation times. We attribute the reduction in rate to the effect of protein synthesis inhibition on the recombinational repair pathway, because this pathway is known to be involved in the repair of both gamma-ray and UV damage. The recovery that took place at the slower rate must reflect a caffeine-sensitive pathway which is involved only in repair of gamma-ray damage and which does not require post-irradiation protein synthesis for activity.
D001203:Ascomycota / Q000528:radiation effects*; D002110:Caffeine / Q000494:pharmacology*; D003513:Cycloheximide / Q000494:pharmacology*; D004260:DNA Repair / Q000187:drug effects*; D005720:Gamma Rays; D014176:Protein Biosynthesis; D011831:Radiation Genetics; D012568:Schizosaccharomyces / Q000187:drug effects / Q000528:radiation effects*; D014466:Ultraviolet Rays
D002110:Caffeine; D003513:Cycloheximide