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

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.
AuthorsTakeki Shiga, Hiroyuki Suzuki, Ayumi Yamamoto, Hiroaki Yamamoto, Kazuo Yamamoto
JournalJournal of radiation research (J Radiat Res) Vol. 51 Issue 4 Pg. 405-15 ( 2010) ISSN: 1349-9157 [Electronic] England
PMID20467201 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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
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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