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Title: Enhanced lysosomal degradation maintains the quiescent state of neural stem cells
Authors: Kobayashi, Taeko
Piao, Wenhui
Takamura, Toshiya
Kori, Hiroshi
Miyachi, Hitoshi
Kitano, Satsuki
Iwamoto, Yumiko
Yamada, Mayumi
Imayoshi, Itaru
Shioda, Seiji
Ballabio, Andrea
Kageyama, Ryoichiro
Author's alias: 小林, 妙子
朴, 文惠
郡, 宏
宮地, 均
北野, さつき
山田, 真弓
今吉, 格
塩田, 清二
影山, 龍一郎
Keywords: Molecular neuroscience
Neural stem cells
Quiescence
Stem cells in the nervous system
Issue Date: 29-Nov-2019
Publisher: Springer Nature
Journal title: Nature Communications
Volume: 10
Thesis number: 5446
Abstract: Quiescence is important for sustaining neural stem cells (NSCs) in the adult brain over the lifespan. Lysosomes are digestive organelles that degrade membrane receptors after they undergo endolysosomal membrane trafficking. Enlarged lysosomes are present in quiescent NSCs (qNSCs) in the subventricular zone of the mouse brain, but it remains largely unknown how lysosomal function is involved in the quiescence. Here we show that qNSCs exhibit higher lysosomal activity and degrade activated EGF receptor by endolysosomal degradation more rapidly than proliferating NSCs. Chemical inhibition of lysosomal degradation in qNSCs prevents degradation of signaling receptors resulting in exit from quiescence. Furthermore, conditional knockout of TFEB, a lysosomal master regulator, delays NSCs quiescence in vitro and increases NSC proliferation in the dentate gyrus of mice. Taken together, our results demonstrate that enhanced lysosomal degradation is an important regulator of qNSC maintenance.
Description: リソソームが成体神経幹細胞を制御するメカニズムを解明. 京都大学プレスリリース. 2019-12-02.
Rights: © The Author(s) 2019. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
URI: http://hdl.handle.net/2433/244865
DOI(Published Version): 10.1038/s41467-019-13203-4
PubMed ID: 31784517
Related Link: http://www.kyoto-u.ac.jp/ja/research/research_results/2019/191129_1.html
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