Hydrogen peroxide causes RAD9-dependent cell cycle arrest in G2 in Saccharomyces cerevisiae whereas menadione causes G1 arrest independent of RAD9 function.

This study shows differences at the level of cell cycle arrest between the response of yeast cells to hydrogen peroxide and superoxide stress. These include both cell cycle phases at which arrest occurs and the involvement of the RAD9 checkpoint gene. Wild-type and rad9 cells were treated with hydrogen peroxide or the superoxide-generating agent menadione. rad9 mutants were up to 100-fold more sensitive to hydrogen peroxide but not affected in their resistance to menadione. Hydrogen peroxide caused G2-phase arrest, whereas menadione-treated cells arrested in G1. G2 arrest, induced by methyl 2-benzimidazil carbamate, increased cellular resistance to hydrogen peroxide but not to menadione. G1 arrest mediated by alpha-factor caused an increase in survival of wild-type cells treated with menadione but not with hydrogen peroxide. A cdc28 mutant arrested in G1 was significantly more sensitive to hydrogen peroxide than other cdc mutants arrested in later phases, including G2. rad9 cells have normal stationary phase resistance to hydrogen peroxide, the ability to adapt to it, glutathione content and induction of genes via the stress responsive element. Although rad9-dependent G2 arrest is important, other rad9-dependent factors may be involved in the resistance of cells to hydrogen peroxide since arrest in G2 did not make rad9 cells fully resistant.