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Open AccessJournal ArticleDOI

OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion

TLDR
Evidence is provided that Optic Atrophy 1 (OPA1), a profusion dynamin-related protein of the inner mitochondrial membrane mutated in dominant optic atrophy, protects from apoptosis by preventing cytochrome c release independently from mitochondrial fusion.
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This article is published in Cell.The article was published on 2006-07-14 and is currently open access. It has received 1444 citations till now. The article focuses on the topics: Optic Atrophy 1 & Inner mitochondrial membrane.

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Mitochondrial Membrane Permeabilization in Cell Death

TL;DR: Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria, meaning that mitochondria coordinate the late stage of cellular demise.
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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Lorenzo Galluzzi, +186 more
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
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Mitochondria: In Sickness and in Health

TL;DR: This work provides a current view of how mitochondrial functions impinge on health and disease and identifies mitochondrial dysfunction as a key factor in a myriad of diseases, including neurodegenerative and metabolic disorders.
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Mitochondria and cell death: outer membrane permeabilization and beyond

TL;DR: MOMP typically leads to cell death irrespective of caspase activity by causing a progressive decline in mitochondrial function, although cells can survive this under certain circumstances, which may have pathophysiological consequences.
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Mitofusin 2 tethers endoplasmic reticulum to mitochondria

TL;DR: It is shown that mitofusin 2, a mitochondrial dynamin-related protein mutated in the inherited motor neuropathy Charcot–Marie–Tooth type IIa, is enriched at the ER–mitochondria interface, and that it tethers ER to mitochondria, a juxtaposition required for efficient mitochondrial Ca2+ uptake.
References
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Journal ArticleDOI

Mechanisms of cytochrome c release by proapoptotic BCL-2 family members.

TL;DR: Data support a model in which the apoptotic pathway bifurcates following activation of a "BH3 only" family member, and proposed mechanisms by which proapoptotic BCL-2 family members induce cytochrome c release are reviewed.
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Dynamin Undergoes a GTP-Dependent Conformational Change Causing Vesiculation

TL;DR: Data presented here demonstrate that purified recombinant dynamin binds to a lipid bilayer in a regular pattern to form helical tubes that constrict and vesiculate upon GTP addition, suggesting that dynamin alone is sufficient for the formation of constricted necks of coated pits and supports the hypothesis that dynamIn is the force-generating molecule responsible for membrane fission.
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Mitochondrial fusion in human cells is efficient, requires the inner membrane potential, and is mediated by mitofusins.

TL;DR: The results show that human mitochondria represent a single cellular compartment whose exchanges and interconnectivity are dynamically regulated by the balance between continuous fusion and fission reactions.
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