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The regulation of mitochondrial morphology: intricate mechanisms and dynamic machinery.

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TLDR
This review focuses on the current understanding of the mitochondrial morphology machinery in cell homeostasis, apoptosis and neurodegeneration, and the post translational modifications that regulate these processes.
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This article is published in Cellular Signalling.The article was published on 2011-10-01. It has received 252 citations till now. The article focuses on the topics: mitochondrial fusion & Mitochondrion.

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Mitochondrial rhomboid parl regulates cytochrome c release during apoptosis via OPA1 dependent cristae remodeling

TL;DR: Parl-associated rhomboid-like (PARL-like) as mentioned in this paper is an inner mitochondrial membrane rhomboids of unknown function, whose yeast ortholog is involved in mitochondrial fusion.
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hFis1, a novel component of the mammalian mitochondrial fission machinery. Vol. 278 (2003) 36373–36379

TL;DR: In this article, the authors identified a mammalian protein called hFis1, which is the orthologue of the yeast Fis1p known to participate in yeast mitochondrial division, and when overexpressed in various cell types, localized to the outer mitochondrial membrane and induced mitochondrial fission.
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Bioenergetic role of mitochondrial fusion and fission.

TL;DR: Fragmented mitochondria are frequently found in resting cells, and mitochondrial fission plays an important role in the removal of damaged organelles by autophagy, which contributes to maintenance of mitochondrial function and optimize bioenergetic capacity.
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Cellular and molecular mechanisms of mitochondrial function

TL;DR: Mitochondria are membrane bound organelles present in almost all eukaryotic cells and contribute to many processes central to cellular function and dysfunction including calcium signalling, cell growth and differentiation, cell cycle control and cell death.
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Impaired mitochondrial function in psychiatric disorders.

TL;DR: There is a growing body of evidence to suggest that impaired mitochondrial function may affect key cellular processes, thereby altering synaptic functioning and contributing to the atrophic changes that underlie the deteriorating long-term course of these illnesses.
References
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Journal ArticleDOI

Mutant huntingtin aggregates impair mitochondrial movement and trafficking in cortical neurons.

TL;DR: It is shown that in cortical neurons, an early event in HD pathophysiology is the aberrant mobility and trafficking of mitochondria caused by cytosolic Htt aggregates, and mitochondrial trafficking was reduced specifically at sites of aggregation while remaining unaltered in regions lacking aggregates.
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Mitochondrial shape changes: orchestrating cell pathophysiology

TL;DR: The roles of mitochondrial dynamics in cell pathophysiology are discussed and how studying dynamics in the context of the immune system could increase knowledge about the role of dynamics in key signalling cascades is considered.
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Inhibiting Drp1-mediated mitochondrial fission selectively prevents the release of cytochrome c during apoptosis

TL;DR: The observation that inhibiting Drp1-mediated mitochondrial fission prevents the mitochondrial release of soluble OPA1 that was proposed to regulate cristae remodeling and complete cytochrome c release during apoptosis is observed, suggesting that mitochondrial fragmentation is not a prerequisite for apoptosis.
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The division of endosymbiotic organelles.

TL;DR: This work has shown that mitochondria and chloroplasts universally require dynamin-related guanosine triphosphatases to divide, and provides fundamental insights into the molecular events driving the division, and possibly the evolution, of organelles in eukaryotes.
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piRNA-associated germline nuage formation and spermatogenesis require MitoPLD profusogenic mitochondrial-surface lipid signaling.

TL;DR: It is proposed that mitochondrial-surface PA generated by MitoPLD/Zuc recruits or activates nuage components critical for piRNA production, suggesting a mechanism for mitochondrial morphology homeostasis.
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