mTORC1 accelerates retinal development via the immunoproteasome

Ji-Heon Choi, Hong Seok Jo, Soyeon Lim, Hyoung-Tai Kim, Kang Woo Lee, Kyeong Hwan Moon, Taejeong Ha, Sang Soo Kwak, Yeha Kim, Eun Jung Lee, Cheol O. Joe and Jin Woo Kim ()
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Ji-Heon Choi: Korea Advanced Institute of Science and Technology (KAIST)
Hong Seok Jo: Korea Advanced Institute of Science and Technology (KAIST)
Soyeon Lim: Korea Advanced Institute of Science and Technology (KAIST)
Hyoung-Tai Kim: Korea Advanced Institute of Science and Technology (KAIST)
Kang Woo Lee: Korea Advanced Institute of Science and Technology (KAIST)
Kyeong Hwan Moon: Korea Advanced Institute of Science and Technology (KAIST)
Taejeong Ha: Korea Advanced Institute of Science and Technology (KAIST)
Sang Soo Kwak: Korea Advanced Institute of Science and Technology (KAIST)
Yeha Kim: Korea Advanced Institute of Science and Technology (KAIST)
Eun Jung Lee: Korea Advanced Institute of Science and Technology (KAIST)
Cheol O. Joe: Korea Advanced Institute of Science and Technology (KAIST)
Jin Woo Kim: Korea Advanced Institute of Science and Technology (KAIST)

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: Abstract 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.

Date: 2018
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DOI: 10.1038/s41467-018-04774-9

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