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Mitochondrial dynamics and inheritance during cell division, development and disease.

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TLDR
Mechanisms have evolved to regulate mitochondrial segregation during cell division, oogenesis, fertilization and tissue development, as well as to ensure the integrity of these organelles and their DNA, including fusion–fission dynamics, organelle transport, mitophagy and genetic selection of functional genomes.
Abstract
During cell division, it is critical to properly partition functional sets of organelles to each daughter cell. The partitioning of mitochondria shares some common features with that of other organelles, particularly in the use of interactions with cytoskeletal elements to facilitate delivery to the daughter cells. However, mitochondria have unique features - including their own genome and a maternal mode of germline transmission - that place additional demands on this process. Consequently, mechanisms have evolved to regulate mitochondrial segregation during cell division, oogenesis, fertilization and tissue development, as well as to ensure the integrity of these organelles and their DNA, including fusion-fission dynamics, organelle transport, mitophagy and genetic selection of functional genomes. Defects in these processes can lead to cell and tissue pathologies.

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Citations
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Journal ArticleDOI

Mitochondrial Dynamics and Metabolic Regulation.

TL;DR: The ways in which metabolic alterations convey changes in mitochondrial morphology and how disruption of mitochondrial morphology impacts cellular and organismal metabolism are reviewed.
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Mitochondrial ROS Signaling in Organismal Homeostasis

TL;DR: This work reviews mitochondrial ROS-mediated signaling pathways with an emphasis on how they are involved in various basal and adaptive physiological responses that control organismal homeostasis.
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Metabolic regulation of mitochondrial dynamics

TL;DR: This work reviews the dynamic properties of mitochondria, with an emphasis on how these processes respond to cellular signaling events and how they affect metabolism.
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AMP-activated protein kinase mediates mitochondrial fission in response to energy stress

TL;DR: The energy-sensing adenosine monophosphate (AMP)–activated protein kinase (AMPK) is genetically required for cells to undergo rapid mitochondrial fragmentation after treatment with ETC inhibitors and direct pharmacological activation of AMPK was sufficient to rapidly promote mitochondrial fragmentation even in the absence of mitochondrial stress.
Journal ArticleDOI

Mitochondrial dynamics and mitochondrial quality control.

TL;DR: This review discusses the most recent progress on the molecular mechanisms and roles of mitochondrial fission/fusion and mitochondrial motility in mitophagy, and discusses multiple pathways leading to the quality control of mitochondria in addition to the traditionalMitophagy pathway under different conditions.
References
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Journal ArticleDOI

Parkin is recruited selectively to impaired mitochondria and promotes their autophagy

TL;DR: It is shown that Parkin is selectively recruited to dysfunctional mitochondria with low membrane potential in mammalian cells and this recruitment promotes autophagy of damaged mitochondria and implicate a failure to eliminate dysfunctional mitochondira in the pathogenesis of Parkinson's disease.
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Mitochondrial Fission, Fusion, and Stress

TL;DR: In their Perspective, Hoppins and Nunnari explain that the endoplasmic reticulum is an active participant in mitochondrial division and discuss how mitochondrial dynamics and cell death are linked.
Journal ArticleDOI

PINK1 is selectively stabilized on impaired mitochondria to activate Parkin.

TL;DR: The authors suggest that PINK1 and Parkin form a pathway that senses damaged mitochondria and selectively targets them for degradation.
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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.
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