mTORC1 accelerates retinal development via the immunoproteasome

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The numbers and types of cells constituting vertebrate neural tissues are determined by cellular mechanisms that couple neurogenesis to the proliferation of neural progenitor cells. Here we identified a role of mammalian target of rapamycin complex 1 (mTORC1) in the development of neural tissue, showing that it accelerates progenitor cell cycle progression and neurogenesis in mTORC1-hyperactive tuberous sclerosis complex 1 (Tsc1)-deficient mouse retina. We also show that concomitant loss of immunoproteasome subunit Psmb9, which is induced by Stat1 (signal transducer and activator of transcription factor 1), decelerates cell cycle progression of Tsc1-deficient mouse retinal progenitor cells and normalizes retinal developmental schedule. Collectively, our results establish a developmental role for mTORC1, showing that it promotes neural development through activation of protein turnover via a mechanism involving the immunoproteasome.
Publisher
NATURE PUBLISHING GROUP
Issue Date
2018-06
Language
English
Article Type
Article
Keywords

CELL-PROLIFERATION; MAMMALIAN PROTEIN; RAT RETINA; RAPAMYCIN; COMPLEX; DROSOPHILA; GROWTH; MICE; GENE; TRANSCRIPTION

Citation

NATURE COMMUNICATIONS, v.9

ISSN
2041-1723
DOI
10.1038/s41467-018-04774-9
URI
http://hdl.handle.net/10203/244563
Appears in Collection
BS-Journal Papers(저널논문)
Files in This Item
Choi JH_Nature Comm.pdf(8.6 MB)Download
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