| アイテムタイプ |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2025-12-08 |
| タイトル |
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タイトル |
Impairment in global protein synthesis uncouples UPR gene induction from HAC1 mRNA splicing in Saccharomyces cerevisiae |
| 言語 |
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言語 |
eng |
| キーワード |
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主題Scheme |
Other |
|
主題 |
yeast |
| キーワード |
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主題Scheme |
Other |
|
主題 |
stress response |
| キーワード |
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主題Scheme |
Other |
|
主題 |
endoplasmic reticulum |
| キーワード |
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主題Scheme |
Other |
|
主題 |
ethanol |
| キーワード |
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主題Scheme |
Other |
|
主題 |
unfolded protein response |
| 資源タイプ |
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資源タイプ |
journal article |
| アクセス権 |
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アクセス権 |
open access |
| 著者 |
Geronimo, Ralph Allen Capistrano
木俣, 有紀
Funahashi, Yutaka
Izawa, Shingo
木俣, 行雄
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| 抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
Upon dysfunction of the endoplasmic reticulum (ER), also known as ER stress, eukaryotic cells alter their transcriptomes. This cytoprotective response is called the unfolded protein response (UPR), which is mediated by Ire1 and HAC1 in the yeast Saccharomyces cerevisiae. ER stress induces self-association and activation of the ER-resident transmembrane endoribonuclease Ire1, which catalyzes the splicing of HAC1 mRNA. It is widely accepted that HAC1 mRNA is translated into the nuclear transcription factor Hac1, only after being spliced. To investigate the cellular response to ethanol-induced ER stress, here we gradually added ethanol into S. cerevisiae cultures until reaching a final concentration of 16%. Unlike conventional ER stressors, such as tunicamycin and dithiothreitol (DTT), the ethanol exposure did not elicit the Ire1- and HAC1-dependent UPR gene induction, even though Ire1 was activated and HAC1-mRNA was efficiently spliced. Under the ethanol stress condition, global protein synthesis was nearly abolished, and the Hac1 protein level remained low, despite the presence of spliced HAC1 mRNA. Furthermore, treatment with the translation inhibitor cycloheximide abolished DTT-induced UPR gene induction. As the UPR signaling pathway requires translation of the spliced HAC1 mRNA, integrity of the translation machinery is deduced to be essential for UPR gene induction. In summary, we demonstrated that impairment of the translation machinery can actually block UPR gene induction under certain stress conditions. We also propose that this represents an advantageous regulatory system that prevents unnecessary gene induction. |
| 書誌情報 |
en : Frontiers in Microbiology
巻 16,
p. 1-15,
ページ数 15,
発行日 2025-09-01
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| 出版者 |
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出版者 |
Frontiers Media |
| ISSN |
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収録物識別子タイプ |
EISSN |
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収録物識別子 |
1664-302X |
| 出版者版DOI |
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関連タイプ |
isReplacedBy |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.3389/fmicb.2025.1629132 |
| 出版者版URI |
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関連タイプ |
isReplacedBy |
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|
識別子タイプ |
URI |
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|
関連識別子 |
https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2025.1629132/full |
| 権利 |
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|
権利情報Resource |
https://creativecommons.org/licenses/by/4.0/ |
|
権利情報 |
© 2025 Geronimo, Ishiwata-Kimata, Funahashi, Izawa and Kimata. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
| 著者版フラグ |
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出版タイプ |
NA |
| 助成情報 |
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助成機関名 |
Japan Society for the Promotion of Science (JSPS) |
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研究課題番号 |
23H02174 |
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研究課題番号URI |
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23K26867/ |
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研究課題名 |
酵母小胞体膜上でのmRNA共局在のメカニズム解明と有用蛋白質産生への応用 |
| 助成情報 |
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助成機関名 |
Japan Society for the Promotion of Science (JSPS) |
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研究課題番号 |
22K19135 |
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研究課題番号URI |
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22K19135/ |
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研究課題名 |
酵母小胞体の形状およびサイズ変化による分泌蛋白質生産能の向上 |
