Impaired Mitochondrial Dynamics And Mitophagy In Neuronal Models Of Tuberous Sclerosis Complex

(Cell Reports 17, 1053–1070; October 18, 2016) We thank R. Kleiman, J. Micozzi, X. Yang, E. Ercan, E. Chadwick, S. Lammers, S. Schaeffer, C. Super (Boston Children’s Hospital [BCH]), and D.J. Kwiatkowski (Brigham and Women’s Hospital) for helpful discussions and technical assistance. We are also grateful to A. Hill and the IDDRC Cellular Imaging Core (funded by NIH P30HD18655) at BCH for technical support and to G. Ashrafi, G. Pekkurnaz, and T.L. Schwarz (BCH) for sharing reagents, software and advice. This work was supported by the Graduate Academy (D.E.-F.) and the Young Investigator Award Program at Heidelberg University (grant F.206773) (D.E.-F. and L.W.), the Daimler & Benz Foundation (grant 32-05/13) (D.E.-F.), the Reinhard-Frank Foundation (D.E.-F.), the German National Academic Foundation (A.S.), the Nancy Lurie Marks Family Foundation, and the Boston Children’s Hospital Translational Research Program (M.S.). C.C. and J.M.R. are affiliated with of LAM Therapeutics. Other research projects in the Sahin Laboratory are supported by Novartis and Pfizer. As a result of an editorial office oversight in the originally published version of this article, the sentence in the Acknowledgements section reads: “Christopher Conrad (C.C.) and Jonathan M. Rothberg (J.M.R.) are employees of LAM Therapeutics.” This error has now been corrected in the article online to read: “C.C. and J.M.R. are affiliated with LAM Therapeutics.” The editorial office apologizes for the error and any inconvenience that may have resulted. Impaired Mitochondrial Dynamics and Mitophagy in Neuronal Models of Tuberous Sclerosis ComplexEbrahimi-Fakhari et al.Cell ReportsOctober 18, 2016In BriefEbrahimi-Fakhari et al. show that mitochondrial dynamics and mitophagy are impaired in neuronal models of tuberous sclerosis complex. Axonal transport, turnover, and presynaptic capturing of mitochondria are compromised. Enhancing autophagic flux through mTORC1-dependent and -independent mechanisms restores mitochondrial homeostasis. Full-Text PDF Open Access