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The Role of Mitochondrial Retrograde...

Munkacsy, Erin Elizabeth.

The Role of Mitochondrial Retrograde Signaling in the Lifespan Extension of Caenorhabditis Elegans.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The Role of Mitochondrial Retrograde Signaling in the Lifespan Extension of Caenorhabditis Elegans.
作者:	Munkacsy, Erin Elizabeth.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, 2017
面頁冊數:	105 p.
附註:	Source: Dissertation Abstracts International, Volume: 78-10(E), Section: B.
附註:	Adviser: Nicholas Musi.
Contained By:	Dissertation Abstracts International78-10B(E).
標題:	Cellular biology.
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10253990
ISBN:	9781369813906

The Role of Mitochondrial Retrograde Signaling in the Lifespan Extension of Caenorhabditis Elegans.
Munkacsy, Erin Elizabeth.

The Role of Mitochondrial Retrograde Signaling in the Lifespan Extension of Caenorhabditis Elegans. - Ann Arbor : ProQuest Dissertations & Theses, 2017 - 105 p.

Source: Dissertation Abstracts International, Volume: 78-10(E), Section: B.

Thesis (Ph.D.)--The University of Texas Health Science Center at San Antonio, 2017.

Mitochondrial dysfunction underlies numerous age-related pathologies. In an effort to discover how the detrimental effects of mitochondrial dysfunction might be alleviated, we examined how the nematode Caenorhabditis elegans not only adapts to disruption of the mitochondrial electron transport chain, but in many instances responds with extended lifespan.

ISBN: 9781369813906Subjects--Topical Terms:

708607
Cellular biology.

The Role of Mitochondrial Retrograde Signaling in the Lifespan Extension of Caenorhabditis Elegans.
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520 $a Mitochondrial dysfunction underlies numerous age-related pathologies. In an effort to discover how the detrimental effects of mitochondrial dysfunction might be alleviated, we examined how the nematode Caenorhabditis elegans not only adapts to disruption of the mitochondrial electron transport chain, but in many instances responds with extended lifespan.
520 $a Altering mitochondrial function changes the relative quantities of metabolites in the cell and may contribute to the resulting organismal phenotype. Some of these metabolites are uniquely enriched in long-lived Caenorhabditis elegans strains with mutations in nuclear-encoded mitochondrial proteins. Specifically, these worms generate elevated amounts of alpha-ketoacids, which are structurally related to alpha-ketoglutarate and may inhibit alpha-ketoglutarate dependent dehydrogenases. We found that provision of several alpha-ketoacids to wild-type worms is sufficient to extend their lifespan and at least one mode of action is through stabilization of hypoxia-inducible factor-1. We also found that an a-ketoglutarate mimetic, 2,4-pyridinedicarboxylic acid, is able to increase the lifespan of wild-type worms but not hypoxia-inducible factor-1 null mutants. Metabolites that build up following mitochondrial respiratory dysfunction may form a novel mode of cell signaling that acts to regulate lifespan.
520 $a In addition, we have identified a novel p38 mitogen-activated protein kinase signaling cascade that is induced by disruption of mitochondrial electron transport chain but independent of the mitochondrial unfolded protein response. This novel cascade is generally activated in counterpoint to the worm ortholog of mammalian nuclear factor-erythroid-related factor, which we show is under the control of the activating transcription factor associated with stress. Significantly, we show that those forms of mitochondrial disruption that activate this mitogen-activated protein kinase cascade induce life extension dependent upon this pathway.
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