Abstract
The major part of the substantial γ-resistance of wild-type Schizosaccharomyces pombe appears to be due to prereplicative recombinational repair mechanisms. The existence of a second “prereplicative G2” repair pathway, specific for γ-induced damage, has now been deduced from studies of the effect of the repair inhibitor caffeine on γ-irradiated G1 phase and G2 phase cells. Only G2 cells are additionally inactivated on exposure to caffeine after γ-irradiation. This shows that both known caffeine-sensitive γ-repair processes (Gentner and Werner, Molec. gen. Genet. 145, 1–5 [1976]) are dependent on the presence of a duplicated genome (2c) at the time of radiation exposure. Pathway I is the known “prereplicative G2” repair process (Fabre, Radiation Res. 56, 528–539 [1973]) which is involved in both UV- and γ-repair, and which requires post-irradiation protein synthesis for activity. Pathway II represents a second distinct “prereplicative G2” repair mechanism; it differs from the first in that it is specific for repair of γ-induced damage and appears to be constitutive.

This publication has 23 references indexed in Scilit: