Detail of SuppFig4e_DG_10z



Project
Title
Immunohistochemistry images of Lamp1, cathepsin B (CtsB), and cathepsin L (CtsL) in the DG in 6-month-old GFAP-GFP;Nestin-NLS-mCherry C57BL/6JJcl Tg mice.
Description
Immunohistochemistry images of Lamp1, cathepsin B (CtsB), and cathepsin L (CtsL) in the DG in 6-month-old GFAP-GFP;Nestin-NLS-mCherry C57BL/6JJcl Tg mice.
Release, Updated
2022-03-31
License
CC BY
Kind
Image data
File Formats
.czi
Data size
5.6 MB

Organism
Mus musculus ( NCBI:txid10090 )
Strain(s)
-
Cell Line
-
Gene symbols
Lamp1, CtsB, CtsL
Protein names
GFAP, Nestin
Protein tags
GFP, mCherry

Datatype
-
Molecular Function (MF)
-
Biological Process (BP)
negative regulation of lysosomal protein catabolic process ( GO:1905166 )
Cellular Component (CC)
lysosome ( GO:0005764 )
Biological Imaging Method
confocal microscopy ( Fbbi:00000251 )
X scale
0.9225176 micrometer/pixel
Y scale
0.9225176 micrometer/pixel
Z scale
1 micrometer/slice
T scale
-

Image Acquisition
Experiment type
-
Microscope type
-
Acquisition mode
-
Contrast method
-
Microscope model
-
Detector model
-
Objective model
-
Filter set
-

Summary of Methods
See details in Kobayashi T, et. al. (2019) Nat Commun., 10(1):5446.
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
Taeko Kobayashi, Ryoichiro Kageyama , Kyoto University, Kyoto University , Institute for Frontier Life and Medical Sciences, Institute for Frontier Life and Medical Sciences
Contributors

OMERO Dataset
OMERO Project
Source