Journal
SCIENCE
Volume 359, Issue 6382, Pages 1416-1421Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aan1053
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Funding
- European Research Council
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- Minerva Foundation
- Israel Science Foundation [1284/13]
- Department of Defense Congressionally Mandated Research Program [W81XWH-2013-1-308 OR120042]
- National Institutes of Health [R01-NS041596, GM103481]
- Company of Biologists
- Koshland senior postdoctoral fellowship
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P41GM103481] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS089633, R01NS041596] Funding Source: NIH RePORTER
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How is protein synthesis initiated locally in neurons? We found that mTOR (mechanistic target of rapamycin) was activated and then up-regulated in injured axons, owing to local translation of mTOR messenger RNA (mRNA). This mRNA was transported into axons by the cell size-regulating RNA-binding protein nucleolin. Furthermore, mTOR controlled local translation in injured axons. This included regulation of its own translation and that of retrograde injury signaling molecules such as importin beta 1 and STAT3 (signal transducer and activator of transcription 3). Deletion of the mTOR 3' untranslated region (3'UTR) in mice reduced mTOR in axons and decreased local translation after nerve injury. Both pharmacological inhibition of mTOR in axons and deletion of the mTOR 3'UTR decreased proprioceptive neuronal survival after nerve injury. Thus, mRNA localization enables spatiotemporal control of mTOR pathways regulating local translation and long-range intracellular signaling.
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