Sebastien Paillusson, Radu Stoica, Patricia Gomez-Suaga, Dawn H. W

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There's Something Wrong with my MAM; the ER–Mitochondria Axis and Neurodegenerative Diseases  Sebastien Paillusson, Radu Stoica, Patricia Gomez-Suaga, Dawn H.W. Lau, Sarah Mueller, Tanya Miller, Christopher C.J. Miller  Trends in Neurosciences  Volume 39, Issue 3, Pages 146-157 (March 2016) DOI: 10.1016/j.tins.2016.01.008 Copyright © 2016 The Authors Terms and Conditions

Figure 1 Electron Microscope Images of Endoplasmic Reticulum (ER)-–Mitochondria Contacts in NSC34 Motor Neuron Cells. A control cell is shown (CTRL) (A) along with a cell transfected with the tethering proteins vesicle-associated membrane protein-associated protein B (VAPB) and protein tyrosine phosphatase interacting protein 51 (PTPIP51) (B) [32]. Some selected ER–mitochondria associations are highlighted in red. Transfection of VAPB and PTPIP51 dramatically increases ER–mitochondria associations. (C) A high-magnification image of a mitochondrion with associated ER in a VAPB/PTPIP51 co-transfected cell; putative tethering structures are discernible connecting the two organelles (arrowheads). Scale bars=500nm (A,B) and 100nm (C). Trends in Neurosciences 2016 39, 146-157DOI: (10.1016/j.tins.2016.01.008) Copyright © 2016 The Authors Terms and Conditions

Figure 2 Proposed Endoplasmic Reticulum (ER)–Mitochondria Tethering Protein Complexes. (A) Inositol 1,4,5-trisphosphate (IP3) receptors (IP3R) and voltage-dependent anion channel (VDAC) interact via GRP75. (B) ER-located mitofusin 2 interacts with mitochondrial mitofusin1/2 (Mfn1, Mfn2). (C) Vesicle-associated membrane protein-associated protein B (VAPB) binds to protein tyrosine phosphatase interacting protein 51 (PTPIP51). (D) (Bap31) binds to Fission 1 homologue (Fis1). Trends in Neurosciences 2016 39, 146-157DOI: (10.1016/j.tins.2016.01.008) Copyright © 2016 The Authors Terms and Conditions

Figure 3 Tar DNA-Binding Protein 43 (TDP-43) Loosens Endoplasmic Reticulum (ER)–Mitochondria Associations in Amyotrophic Lateral Sclerosis with Associated Frontotemporal Dementia (ALS/FTD). (A) Normal situation. (B) Disease situation. TDP-43 induces activation glycogen synthase kinase 3β (GSK-3β), which then disrupts binding of vesicle-associated membrane protein-associated protein B (VAPB) to protein tyrosine phosphatase interacting protein 51 (PTPIP51) to reduce ER–mitochondria associations and Ca2+ exchange between the two organelles. Trends in Neurosciences 2016 39, 146-157DOI: (10.1016/j.tins.2016.01.008) Copyright © 2016 The Authors Terms and Conditions

Figure 4 Disruption to Endoplasmic Reticulum (ER)–Mitochondria Associations Provides a Mechanism by which many of the Disparate Pathological Features of Neurodegenerative Diseases Might Arise. Trends in Neurosciences 2016 39, 146-157DOI: (10.1016/j.tins.2016.01.008) Copyright © 2016 The Authors Terms and Conditions