Summary of ssbd-repos-000189

SSBD:database
URL

Name
ssbd-repos-000189 (189-Kobayashi-NSCsDyn)
URL
DOI
-

Title
Confocal microscopy images of lysosomes situation in NSCs in both the DG and SVZ of mice.
Description
-
Submited Date
-
Release Date
2022-03-31
Updated Date
-
License
Funding information
-
File formats
Data size
6.8 GB

Organism
Mus musculus
Strain
-
Cell Line
-
Genes
CtsB, CtsL, Lamp1
Proteins
GFAP, Nestin, TFEB, caTFEB

GO Molecular Function (MF)
NA
GO Biological Process (BP)
cell division, negative regulation of lysosomal protein catabolic process
GO Cellular Component (CC)
lysosome, NA
Study Type
Notch/metabolism, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Adult Stem Cells/metabolism, Dentate Gyrus/metabolism, Lysosomes, Proteostasis, Mice, Receptors, Endosomes, Knockout, Animals, Adult Stem Cells, ErbB Receptors, Lysosomes/metabolism, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics, Proteolysis, ErbB Receptors/metabolism, Neural Stem Cells, Notch, Dentate Gyrus, Endosomes/metabolism, Neural Stem Cells/metabolism
Imaging Methods
confocal microscopy

Method Summary
-
Related paper(s)

Taeko Kobayashi, Wenhui Piao, Toshiya Takamura, Hiroshi Kori, Hitoshi Miyachi, Satsuki Kitano, Yumiko Iwamoto, Mayumi Yamada, Itaru Imayoshi, Seiji Shioda, Andrea Ballabio, Ryoichiro Kageyama (2019) Enhanced lysosomal degradation maintains the quiescent state of neural stem cells., Nature communications, Volume 10, Number 1, pp. 5446

Published in 2019 Nov 29 (Electronic publication in Nov. 29, 2019, midnight )

(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.
(MeSH Terms)

Contact(s)
Taeko Kobayashi, Ryoichiro Kageyama
Organization(s)
Kyoto University, Kyoto University , Institute for Frontier Life and Medical Sciences, Institute for Frontier Life and Medical Sciences
Image Data Contributors
Quantitative Data Contributors

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