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  Reduced insulin signaling maintains electrical transmission in a neural circuit in aging flies

Augustin, H., McGourty, K., Allen, M. J., Madem, S. K., Adcott, J., Kerr, F., et al. (2017). Reduced insulin signaling maintains electrical transmission in a neural circuit in aging flies. PLoS Biol, 15(9), e2001655. doi:10.1371/journal.pbio.2001655.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0001-58EE-1 Version Permalink: http://hdl.handle.net/21.11116/0000-0001-58EF-0
Genre: Journal Article

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Augustin, H.1, Author
McGourty, K.1, Author
Allen, M. J.1, Author
Madem, S. K.1, Author
Adcott, J.1, Author
Kerr, F.1, Author
Wong, C. T.1, Author
Vincent, A.1, Author
Godenschwege, T.1, Author
Boucrot, E.1, Author
Partridge, L.1, Author
Affiliations:
1Max Planck Institute for Biology of Ageing, Max Planck Society, Joseph-Stelzmann-Str. 9b, D-50931 Cologne, DE, ou_1942284              

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Free keywords: Aging/*physiology Animals Connexins/metabolism Drosophila/*physiology Escape Reaction/physiology Female Gap Junctions/physiology Insulin/*metabolism Male Somatomedins/*metabolism *Synaptic Transmission rab GTP-Binding Proteins/metabolism
 Abstract: Lowered insulin/insulin-like growth factor (IGF) signaling (IIS) can extend healthy lifespan in worms, flies, and mice, but it can also have adverse effects (the "insulin paradox"). Chronic, moderately lowered IIS rescues age-related decline in neurotransmission through the Drosophila giant fiber system (GFS), a simple escape response neuronal circuit, by increasing targeting of the gap junctional protein innexin shaking-B to gap junctions (GJs). Endosomal recycling of GJs was also stimulated in cultured human cells when IIS was reduced. Furthermore, increasing the activity of the recycling small guanosine triphosphatases (GTPases) Rab4 or Rab11 was sufficient to maintain GJs upon elevated IIS in cultured human cells and in flies, and to rescue age-related loss of GJs and of GFS function. Lowered IIS thus elevates endosomal recycling of GJs in neurons and other cell types, pointing to a cellular mechanism for therapeutic intervention into aging-related neuronal disorders.

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 Dates: 2017
 Publication Status: Published in print
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 Rev. Type: -
 Identifiers: Other: 28902870
DOI: 10.1371/journal.pbio.2001655
ISSN: 1545-7885 (Electronic)1544-9173 (Linking)
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Title: PLoS Biol
Source Genre: Journal
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Pages: - Volume / Issue: 15 (9) Sequence Number: - Start / End Page: e2001655 Identifier: -