Requirement of peroxiredoxin on the stationary phase of yeast cell growth
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- Watanabe Toshihiko
- Department of Microbiology, Tohoku Pharmaceutical University
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- Irokawa Hayato
- Department of Microbiology, Tohoku Pharmaceutical University
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- Ogasawara Ayako
- Department of Microbiology, Tohoku Pharmaceutical University
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- Iwai Kenta
- Department of Microbiology, Tohoku Pharmaceutical University
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- Kuge Shusuke
- Department of Microbiology, Tohoku Pharmaceutical University
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抄録
Toxic chemicals often induce reactive oxygen species (ROS). Although one of the most abundant ROS-sensitive proteins is in the peroxiredoxin (Prx) family, the function of Prx proteins is poorly understood because they are inactivated under high concentrations of hydrogen peroxide. Like mammalian cells, the model eukaryote Saccharomyces cerevisiae possesses multiple Prx proteins. Among the five Prx family proteins, Tsa1 and Ahp1 have the highest and second-highest expression levels, respectively. Here, we focused on a previously uncharacterized phenotype resulting from Tsa1 loss: impaired growth during the late exponential phase. We overexpressed catalase (CTT1) and Ahp1 in cells with disruptions in TSA1 and its homologue, TSA2 (tsa1/2Δ cells), and we found that neither Ctt1 nor Ahp1 overexpression suppressed the impaired cell growth at the stationary phase, although the ROS levels were successfully suppressed. Furthermore, the cell cycle profile was not altered by Tsa1/2 loss, at least in the late exponential phase; however, the glucose consumption rate slowed in the late exponential phase. Our results suggest that ROS levels are not responsible for the growth phenotype. Tsa1 might have a specific function that could not be replaced by Ahp1.
収録刊行物
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- The Journal of Toxicological Sciences
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The Journal of Toxicological Sciences 39 (1), 51-58, 2014
一般社団法人 日本毒性学会
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詳細情報 詳細情報について
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- CRID
- 1390001204904071296
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- NII論文ID
- 130004447114
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- NII書誌ID
- AN00002808
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- COI
- 1:STN:280:DC%2BC2czkvFSmtg%3D%3D
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- ISSN
- 18803989
- 03881350
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- NDL書誌ID
- 025244041
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- PubMed
- 24418709
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 使用不可