| The retrograde response: when mitochondrial quality control is not enough. | |
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MedLine Citation:
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PMID: 22374136 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Mitochondria are responsible for generating adenosine triphosphate (ATP) and metabolic intermediates for biosynthesis. These dual functions require the activity of the electron transport chain in the mitochondrial inner membrane. The performance of these electron carriers is imperfect, resulting in release of damaging reactive oxygen species. Thus, continued mitochondrial activity requires maintenance. There are numerous means by which this quality control is ensured. Autophagy and selective mitophagy are among them. However, the cell inevitably must compensate for declining quality control by activating a variety of adaptations that entail the signaling of the presence of mitochondrial dysfunction to the nucleus. The best known of these is the retrograde response. This signaling pathway is triggered by the loss of mitochondrial membrane potential, which engages a series of signal transduction proteins, and it culminates in the induction of a broad array of nuclear target genes. One of the hallmarks of the retrograde response is its capacity to extend the replicative life span of the cell. The retrograde signaling pathway interacts with several other signaling pathways, such as target of rapamycin (TOR) and ceramide signaling. All of these pathways respond to stress, including metabolic stress. The retrograde response is also linked to both autophagy and mitophagy at the gene and protein activation levels. Another quality control mechanism involves age-asymmetry in the segregation of dysfunctional mitochondria. One of the processes that impinge on this age-asymmetry is related to biogenesis of the organelle. Altogether, it is apparent that mitochondrial quality control constitutes a complex network of processes, whose full understanding will require a systems approach. This article is part of a Special Issue entitled: Protein Import and Quality Control in Mitochondria and Plastids. |
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Authors:
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S Michal Jazwinski |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2012-02-21 |
Journal Detail:
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Title: Biochimica et biophysica acta Volume: 1833 ISSN: 0006-3002 ISO Abbreviation: Biochim. Biophys. Acta Publication Date: 2013 Feb |
Date Detail:
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Created Date: 2012-12-24 Completed Date: 2013-03-19 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 0217513 Medline TA: Biochim Biophys Acta Country: Netherlands |
Other Details:
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Languages: eng Pagination: 400-9 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier B.V. All rights reserved. |
Affiliation:
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Tulane Center for Aging and Department of Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112, USA. sjazwins@tulane.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Mitochondria
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metabolism* Protein Transport Quality Control Saccharomyces cerevisiae / metabolism* Saccharomyces cerevisiae Proteins / metabolism* Signal Transduction |
| Grant Support | |
ID/Acronym/Agency:
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R01 AG017887-06/AG/NIA NIH HHS; R37 AG006168/AG/NIA NIH HHS; R37 AG006168-24/AG/NIA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Saccharomyces cerevisiae Proteins |
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