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Publication : mTORC1 accelerates retinal development via the immunoproteasome.

First Author  Choi JH Year  2018
Journal  Nat Commun Volume  9
Issue  1 Pages  2502
PubMed ID  29950673 Mgi Jnum  J:266104
Mgi Id  MGI:6208931 Doi  10.1038/s41467-018-04774-9
Citation  Choi JH, et al. (2018) mTORC1 accelerates retinal development via the immunoproteasome. Nat Commun 9(1):2502
abstractText  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.
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