OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion
Christian Frezza,Sara Cipolat,Olga Martins de Brito,Massimo Micaroni,Galina V. Beznoussenko,Tomasz Rudka,Davide Bartoli,Roman S. Polishuck,Nika N. Danial,Bart De Strooper,Luca Scorrano +10 more
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.About:
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.read more
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The Metabolomic Signature of Opa1 Deficiency in Rat Primary Cortical Neurons Shows Aspartate/Glutamate Depletion and Phospholipids Remodeling.
Juan Manuel Chao de la Barca,Macarena S. Arrázola,Macarena S. Arrázola,Cinzia Bocca,Laetitia Arnauné-Pelloquin,Olga Iuliano,Guillaume Tcherkez,Guy Lenaers,Gilles Simard,Pascale Belenguer,Pascal Reynier +10 more
TL;DR: Target metabolomics on rat cortical neurons with OPA1 expression inhibited by RNA interference revealed 6 significantly different metabolites in OPA2 down-regulated neurons, with aspartate being the most significant (p < 0.001) and the phospholipid signature may reflect intracellular membrane remodeling due to loss of mitochondrial fusion and/or lipid droplet accumulation.
Posted ContentDOI
A surface morphometrics toolkit to quantify organellar membrane ultrastructure using cryo-electron tomography
TL;DR: In this paper , a suite of ultrastructural quantifications, integrated into a single pipeline called the surface morphometrics toolkit, is presented, allowing detailed mapping of spacing, curvature, and orientation onto reconstructed membrane meshes, highlighting subtle organellar features that are challenging to detect in 3D.
Journal ArticleDOI
Modeling the Effects of Calcium Overload on Mitochondrial Ultrastructural Remodeling.
Jasiel O. Strubbe-Rivera,Jiahui Chen,Benjamin A. West,Kristin N. Parent,Guo-Wei Wei,Jason N. Bazil +5 more
TL;DR: In this paper, a phase-based separation approach of both the inner membrane space and matrix space is presented to understand how cristae are formed using the Cahn-Hilliard equation.
Journal ArticleDOI
Carboxyl-terminal modulator protein induces apoptosis by regulating mitochondrial function in lung cancer cells
Soon-Kyung Hwang,Arash Minai-Tehrani,Kyeong-Nam Yu,Seung-Hee Chang,Ji-Eun Kim,Kee-Ho Lee,Jongsun Park,George R. Beck,Myung-Haing Cho +8 more
TL;DR: Examination of the role of CTMP in mitochondrial-mediated apoptosis and regulation of mitochondrial function in human lung carcinoma cells showed that CTMP altered mitochondrial morphology and caused the release of cytochrome c by inhibiting OPA1 expression.
References
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Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death
Michael C. Wei,Michael C. Wei,Wei-Xing Zong,Emily H. Cheng,Tullia Lindsten,Vily Panoutsakopoulou,Andrea J. Ross,Kevin A. Roth,Grant R. MacGregor,Craig B. Thompson,Stanley J. Korsmeyer +10 more
TL;DR: In this article, the authors found that doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin.
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The Pathophysiology of Mitochondrial Cell Death
Douglas R. Green,Guido Kroemer +1 more
TL;DR: The therapeutic induction of MOMP may restore apoptosis in cancer cells in which it is disabled, and the general rules governing the pathophysiology and controversial issues regarding its regulation are discussed.
Journal ArticleDOI
Two CD95 (APO-1/Fas) signaling pathways
Carsten Scaffidi,Simone Fulda,Anu Srinivasan,Claudia Friesen,Feng Li,Kevin J. Tomaselli,Klaus-Michael Debatin,Peter H. Krammer,Marcus E. Peter +8 more
TL;DR: In the presence of caspase‐3 the amount of active casp enzyme‐8 generated at the DISC determines whether a mitochondria‐independent apoptosis pathway is used (type I cells) or not (type II cells).
Journal Article
The expanding role of mitochondria in apoptosis
TL;DR: The complexity of the apoptotic program began to increase with the discovery of Bcl-2, a gene whose product causes resistance to apoptosis in lymphocytes, and the complex role of mitochondria in apoptosis came into focus when biochemical studies identified several mitochondrial proteins that are able to activate cellular apoptotic programs directly.
Journal ArticleDOI
Mitofusins Mfn1 and Mfn2 coordinately regulate mitochondrial fusion and are essential for embryonic development
TL;DR: It is concluded that Mfn1 and Mfn2 have both redundant and distinct functions and act in three separate molecular complexes to promote mitochondrial fusion, and by enabling cooperation between mitochondria, has protective effects on the mitochondrial population.