Hydroquinone,a benzene metabolite,induces Hog1-dependent stress response signaling and causes aneuploidyin Saccharomyces cerevisiae

Previously,we have shown that phenyl hydroquinone,a hepatic metabolite of the ames test-negative carcinogen o-phenylphenol,efficiently induced aneuploidy in saccharomyces cerevisiae by arresting the cell cycle at the g2/m transition as a result of the activation of the hog1 (p38 mapk homolog)-swe1 (wee1 homolog) pathway. in this experiment,we examined the aneuploidy forming effects of hydroquinone,a benzene metabolite,since both phenyl hydroquinone and hydroquinone are ames-test negative carcinogens and share similar molecular structures. as was seen in phenyl hydroquinone,hydroquinone induced aneuploidy in yeast by delaying the cell cycle at the g2/m transition. deficiencies in swe1 and hog1 abolished the hydroquinone-induced delay at the g2/m transition and aneuploidy formation. furthermore,hog1 was phosphorylated by hydroquinone,which may stabilize swe1.these data indicate that the hydroquinone-induced g2/m transition checkpoint,which is activated by the hog1-swe1 pathway,plays a role in the formation of aneuploidy.