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β-SNAP activity in the outer segment growth period is critical for preventing BNip1-dependent apoptosis in zebrafish photoreceptors
https://oist.repo.nii.ac.jp/records/1837
https://oist.repo.nii.ac.jp/records/18374eef6275-52cb-4951-acf7-584212334319
名前 / ファイル | ライセンス | アクション |
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Nishiwaki-2020-β-SNAP activity in the outer se (13.4 MB)
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Creative Commons Attribution 4.0 International(https://creativecommons.org/licenses/by/4.0/)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2020-12-09 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | β-SNAP activity in the outer segment growth period is critical for preventing BNip1-dependent apoptosis in zebrafish photoreceptors | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者(英) |
Nishiwaki, Yuko
× Nishiwaki, Yuko× Masai, Ichiro |
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書誌情報 |
en : Scientific Reports 巻 10, 号 1, p. 17379, 発行日 2020-10-15 |
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抄録 | ||||||
内容記述タイプ | Other | |||||
内容記述 | BNip1, which functions as a t-SNARE component of the syntaxin18 complex, is localized on the ER membrane and regulates retrograde transport from Golgi to the ER. BNip1 also has a BH3 domain, which generally releases pro-apoptotic proteins from Bcl2-mediated inhibition. Previously we reported that retinal photoreceptors undergo BNip1-dependent apoptosis in zebrafish β-snap1 mutants. Here, we investigated physiological roles of BNip1-dependent photoreceptor apoptosis. First, we examined the spatio-temporal profile of photoreceptor apoptosis in β-snap1 mutants, and found that apoptosis occurs only during a small developmental window, 2–4 days-post-fertilization (dpf), in which an apical photoreceptive membrane structure, called the outer segment (OS), grows rapidly. Transient expression of β-SNAP1 during this OS growing period prevents photoreceptor apoptosis in β-snap1 mutants, enabling cone to survive until at least 21 dpf. These observations suggest that BNip1-mediated apoptosis is linked to excessive activation of vesicular transport associated with rapid growth of the OS. Consistently, knockdown of Ift88 and Kif3b, which inhibits protein transport to the OS, rescued photoreceptor apoptosis in β-snap1 mutants. Treatment with rapamycin, which inhibits protein synthesis via the mTOR pathway, also rescued photoreceptor apoptosis in β-snap1 mutants. These data suggest that BNip1 performs risk assessment to detect excessive vesicular transport in photoreceptors. | |||||
出版者 | ||||||
出版者 | Nature Research | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 2045-2322 | |||||
PubMed番号 | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | PMID | |||||
関連識別子 | info:pmid/33060680 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | info:doi/10.1038/s41598-020-74360-x | |||||
権利 | ||||||
権利情報 | © 2020 The Author(s). | |||||
関連サイト | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://www.nature.com/articles/s41598-020-74360-x | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |