| ○種別 (必須): | □ | 学術論文 (審査論文)
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| ○言語 (必須): | □ | 英語
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| ○招待 (推奨): |
| ○審査 (推奨): |
| ○カテゴリ (推奨): |
| ○共著種別 (推奨): | □ | 国内共著 (徳島大学内研究者と国内(学外)研究者との共同研究 (国外研究者を含まない))
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| ○学究種別 (推奨): |
| ○組織 (推奨): |
| ○著者 (必須): | 1. | (英) Yamaguchi Junji (日) (読)
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| 2. | (英) Suzuki Chigure (日) (読)
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| 3. | (英) Nanao Tomohisa (日) (読)
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| 4. | (英) Kakuta Soichirou (日) (読)
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| 5. | (英) Ozawa Kentarou (日) (読)
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| 6. | (英) Tanida Isei (日) (読)
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| 7. | 齊藤 達哉
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| 8. | (英) Sunabori Takehiko (日) (読)
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| 9. | (英) Komatsu Masaaki (日) (読)
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| 10. | (英) Tanaka Keiji (日) (読)
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| 11. | (英) Aoki Shigeki (日) (読)
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| 12. | (英) Sakimura Kenji (日) (読)
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| 13. | (英) Uchiyama Yasuo (日) (読)
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| ○題名 (必須): | □ | (英) Atg9a deficiency causes axon-specific lesions including neuronal circuit dysgenesis. (日)
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| ○要約 (任意): | □ | (英) Conditional knockout mice for Atg9a, specifically in brain tissue, were generated to understand the roles of ATG9A in the neural tissue cells. The mice were born normally, but half of them died within one week, and none lived beyond 4 weeks of age. SQSTM1/p62 and NBR1, receptor proteins for selective autophagy, together with ubiquitin, accumulated in Atg9a-deficient neurosoma at postnatal day 15 (P15), indicating an inhibition of autophagy, whereas these proteins were significantly decreased at P28, as evidenced by immunohistochemistry, electron microscopy and western blot. Conversely, degenerative changes such as spongiosis of nerve fiber tracts proceeded in axons and their terminals that were occupied with aberrant membrane structures and amorphous materials at P28, although no clear-cut degenerative change was detected in neuronal cell bodies. Different from autophagy, diffusion tensor magnetic resonance imaging and histological observations revealed Atg9a-deficiency-induced dysgenesis of the corpus callosum and anterior commissure. As for the neurite extensions of primary cultured neurons, the neurite outgrowth after 3 day culturing was significantly impaired in primary neurons from atg9a-KO mouse brains, but not in those from atg7-KO and atg16l1-KO brains. Moreover, this tendency was also confirmed in Atg9a-knockdown neurons under an atg7-KO background, indicating the role of ATG9A in the regulation of neurite outgrowth that is independent of autophagy. These results suggest that Atg9a deficiency causes progressive degeneration in the axons and their terminals, but not in neuronal cell bodies, where the degradations of SQSTM1/p62 and NBR1 were insufficiently suppressed. Moreover, the deletion of Atg9a impaired nerve fiber tract formation. (日)
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| ○キーワード (推奨): |
| ○発行所 (推奨): |
| ○誌名 (必須): | □ | Autophagy ([Taylor & Francis])
(pISSN: 1554-8627, eISSN: 1554-8635)
| ○ISSN (任意): | □ | 1554-8635
ISSN: 1554-8627
(pISSN: 1554-8627, eISSN: 1554-8635) Title: AutophagyTitle(ISO): AutophagyPublisher: Taylor & Francis (NLM Catalog)
(Scopus)
(CrossRef)
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| ○巻 (必須): |
| ○号 (必須): |
| ○頁 (必須): |
| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2017年 5月 17日 (平成 29年 5月 17日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1080/15548627.2017.1314897 (→Scopusで検索)
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| ○PMID (任意): | □ | 28513333 (→Scopusで検索)
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| ○備考 (任意): | 1. | (英) PublicationType: Journal Article (日)
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