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
Citations
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Mitochondrial fission and fusion
Iain Scott,Richard J. Youle +1 more
TL;DR: The mechanisms behind mitochondrial fission and fusion are discussed, and the implications of changes in organelle morphology during the life of a cell are discussed.
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ChChd3, an Inner Mitochondrial Membrane Protein is Essential for Maintaining Cristae Integrity and Mitochondrial Function
Manjula Darshi,Guy Perkins,Mason R. Mackey,Susanna Petrosyan,Anne N. Murphy,Mark H. Ellisman,Susan S. Taylor +6 more
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MICOS coordinates with respiratory complexes and lipids to establish mitochondrial inner membrane architecture
TL;DR: The organization and functional roles of MICOS are addressed and two independent MICOS subcomplexes are identified: Mic27/Mic10/Mic12, whose assembly is dependent on respiratory complexes and the mitochondrial lipid cardiolipin, and Mic60/Mic19, which assembles independent of these factors.
Journal ArticleDOI
Mitochondrial fission/fusion dynamics and apoptosis.
Clare Sheridan,Seamus J. Martin +1 more
TL;DR: Evidence for and against the role of mitochondrial fragmentation in the progression of apoptosis is discussed and recent advances which indicate that mitochondrial fission is not a critical requirement for apoptosis-associated cytochrome c release are highlighted.
Journal ArticleDOI
Maternal metabolic syndrome programs mitochondrial dysfunction via germline changes across three generations
Jessica Saben,Anna L. Boudoures,Zeenat Asghar,Alysha Thompson,Andrea M. Drury,Wendy Zhang,Maggie M.-Y. Chi,Andrew Cusumano,Suzanne M. Scheaffer,Kelle H. Moley +9 more
TL;DR: The results indicate that maternal programming of metabolic disease can be passed through the female germline and that the transfer of aberrant oocyte mitochondria to subsequent generations may contribute to the increased risk for developing insulin resistance.
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.
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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.
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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.