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. 2018 Feb 28;11:64. doi: 10.3389/fnmol.2018.00064

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Copyright © 2018 Perez Carrion, Pischedda, Biosa, Russo, Straniero, Civiero, Guida, Gloeckner, Ticozzi, Tiloca, Mariani, Pezzoli, Duga, Pichler, Pan, Landers, Greggio, Hess, Goldwurm and Piccoli.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The E193K variant prevents mitochondrial fission upon MPP+ treatment. (A) Under basal conditions mitochondria undergo continuous cycles of fusion and fission. Fission requires the activity of DRP1. LRRK2 binds to DRP1 and increases DRP1 recruitment to mitochondria. (B) Under noxious stimuli, WT cells react via the LRRK2-DRP1 complex that allows mitochondrial fission (1). Eventually, damaged mitochondria are eliminated via autophagy (2) limiting the production of ROS. (C) In the presence of a toxic insult the LRRK2 E193K-DRP1 complex is partially destabilized. This leads to an incomplete fragmentation of mitochondria that prevents the clearance of damaged organelles and increases the production of ROS.