Abstract |
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.
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Authors | Takeki Shiga, Hiroyuki Suzuki, Ayumi Yamamoto, Hiroaki Yamamoto, Kazuo Yamamoto |
Journal | Journal of radiation research
(J Radiat Res)
Vol. 51
Issue 4
Pg. 405-15
( 2010)
ISSN: 1349-9157 [Electronic] England |
PMID | 20467201
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Cell Cycle Proteins
- Hydroquinones
- Mutagens
- Saccharomyces cerevisiae Proteins
- SWE1 protein, S cerevisiae
- Checkpoint Kinase 2
- Protein-Tyrosine Kinases
- Protein Serine-Threonine Kinases
- HOG1 protein, S cerevisiae
- Mitogen-Activated Protein Kinases
- RAD53 protein, S cerevisiae
- Benzene
- hydroquinone
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Topics |
- Aneuploidy
- Benzene
(metabolism, toxicity)
- Cell Cycle
(drug effects, genetics)
- Cell Cycle Proteins
(metabolism)
- Checkpoint Kinase 2
- Genes, Fungal
- Hydroquinones
(metabolism, toxicity)
- Mitogen-Activated Protein Kinases
(metabolism)
- Mutagens
(metabolism, toxicity)
- Protein Serine-Threonine Kinases
(metabolism)
- Protein-Tyrosine Kinases
(metabolism)
- Saccharomyces cerevisiae
(cytology, drug effects, genetics, metabolism)
- Saccharomyces cerevisiae Proteins
(metabolism)
- Signal Transduction
(drug effects)
- Stress, Physiological
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