著者
Shiga Takeki Suzuki Hiroyuki Yamamoto Ayumi YAMAMOTO Hiroaki YAMAMOTO Kazuo
出版者
Journal of Radiation Research Editorial Committee
雑誌
Journal of radiation research (ISSN:04493060)
巻号頁・発行日
vol.51, no.4, pp.405-415, 2010-07-16
被引用文献数
1 12

Previously, we have shown that phenyl hydroquinone, a hepatic metabolite of the Ames test-negative carcinogen <i>o</i>-phenylphenol, efficiently induced aneuploidy in <i>Saccharomyces cerevisiae</i> 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 <i>SWE1</i> and <i>HOG1</i> 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.