Science (New York, N.Y.) · 2018
Locally translated mTOR controls axonal local translation in nerve injury.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Terenzio Marco, Koley Sandip, Samra Nitzan, Rishal Ida, Zhao Qian, Sahoo Pabitra K, Urisman Anatoly, Marvaldi Letizia, Oses-Prieto Juan A, Forester Craig, Gomes Cynthia, Kalinski Ashley L, Di Pizio Agostina, Doron-Mandel Ella, Perry Rotem Ben-Tov, Koppel Indrek, Twiss Jeffery L, Burlingame Alma L, Fainzilber Mike
Аннотация
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 β1 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.