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3,6‐Epidioxy‐1,10‐bisaboladiene inhibits G 1 ‐specific transcription through Swi4/Swi6 and Mbp1/Swi6 via the Hog1 stress pathway in yeast
Author(s) -
Imamura Yuko,
Yukawa Masashi,
Ueno Masaru,
Kimura Kenichi,
Tsuchiya Eiko
Publication year - 2014
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.12965
Subject(s) - saccharomyces cerevisiae , transcription factor , biology , immunoprecipitation , p38 mitogen activated protein kinases , mechanism of action , cyclin , microbiology and biotechnology , kinase , signal transduction , phosphorylation , protein kinase a , biochemistry , yeast , apoptosis , gene , cell cycle , in vitro
3,6‐Epidioxy‐1,10‐bisaboladiene ( EDBD ), a bisabolane sesquiterpene endoperoxide compound, was previously isolated from Cacalia delphiniifolia and C. hastata in northern Japan. EDBD has cytotoxic effects and induces apoptosis via phosphorylation of p38 mitogen‐activated protein kinase in human promyelocytic leukemia HL 60 cells. However, the mechanism of action of EDBD has not yet been fully elucidated. In this study, we examined the molecular mechanisms of EDBD in the budding yeast Saccharomyces cerevisiae . EDBD arrested the growth of S. cerevisiae cells by suppressing progression from the G 1 phase to the S phase and from the G 2 phase to the M phase. Moreover, biochemical and genetic analyses revealed that EDBD activated environmental stress–response pathways involving Hog1 and affected Cln3/G 1 cyclin activity, thereby inhibiting the expression of SCB ‐binding factor and MCB ‐binding factor target genes. Our results provided important insights into the functions of EDBD in tumor cells and may facilitate the development of EDBD ‐based antitumor therapies. Structured digital abstract • Swi4 physically interacts with Swi6 by anti tag coimmunoprecipitation ( View interaction )