Decreased insulin-receptor signaling promotes the autophagic degradation of beta-amyloid peptide in C. elegans.

Decreased insulin-receptor signaling promotes the autophagic degradation of beta-amyloid peptide in C. elegans. Research Abstract Details 

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Decreased insulin-receptor signaling promotes the autophagic degradation of beta-amyloid peptide in C. elegans. Abstract Text:

Maria L Florez-McClure,Lindsay A Hohsfield,Gin Fonte,Matthew T Bealor,Christopher D Link,Maria L Florez-McClure,Lindsay A Hohsfield,Gin Fonte,Matthew T Bealor,Christopher D Link,Maria L Florez-McClure,Lindsay A Hohsfield,Gin Fonte,Matthew T Bealor,Christopher D Link,

Autophagy is a conserved membrane trafficking pathway that mediates the delivery of cytoplasmic substrates to the lysosome for degradation. Impaired autophagic function is implicated in the pathology of various neurodegenerative diseases. We have generated transgenic C. elegans that express human beta-amyloid peptide (Abeta) in order to examine the mechanism(s) of Abeta-toxicity. In this model, Abeta expression causes autophagosome accumulation, thereby mimicking a pathology found in brains of Alzheimer's disease patients. Furthermore, we demonstrate that decreased insulin-receptor signaling [using the daf-2(e1370) mutation] suppresses Abeta-induced paralysis by a mechanism that requires autophagy. Surprisingly, the daf-2 mutation also decreases Abeta-induced autophagosome accumulation. These observations can be explained by a model in which decreased insulin-receptor signaling promotes the maturation of autophagosomes into degradative autolysosomes, whereas Abeta impairs this process. Consistent with this model, we find that RNAi-mediated knock-down of lysosomal components results in enhanced Abeta-toxicity and autophagosome accumulation. Also, Abeta; daf-2(e1370) nematodes contain more lysosomes than either Abeta or control strains. Finally, we demonstrate that decreased insulin-receptor signaling promotes the autophagic degradation of Abeta.

Decreased insulin-receptor signaling promotes the autophagic degradation of beta-amyloid peptide in C. elegans. Publishing Authors By Initials

ML Florez-McClure,LA Hohsfield,G Fonte,MT Bealor,CD Link,ML Florez-McClure,LA Hohsfield,G Fonte,MT Bealor,CD Link,ML Florez-McClure,LA Hohsfield,G Fonte,MT Bealor,CD Link,

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MEDLINE DATE: 2007 Nov-Dec

Decreased insulin-receptor signaling promotes the autophagic degradation of beta-amyloid peptide in C. elegans. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Autophagy

VOLUME: 3

Page Numbers: 569-80

Journal Abbreviation: Autophagy

ISSN: 1554-8627

DAY: 20

MONTH: 07

YEAR: 2007

Decreased insulin-receptor signaling promotes the autophagic degradation of beta-amyloid peptide in C. elegans. Information

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LANGUAGE: eng

NlmUniqueID: 101265188

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Grant and Affiliation Information for Decreased insulin-receptor signaling promotes the autophagic degradation of beta-amyloid peptide in C. elegans.

AFFILIATION: Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA. maria.mcclure@colorado.edu

Country: United States

AGENCY: United States NICHD

GRANT: HD007289

ACRONYM: HD

MEDLINETA: Autophagy

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