Item

ITEM ACTIONS

This item is discarded!Release HistoryDetailsSummary

Discarded

Journal Article

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

MPS-Authors

Augustin, H.
Max Planck Institute for Biology of Ageing, Max Planck Society;

McGourty, K.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Allen, M. J.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Madem, S. K.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Adcott, J.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Kerr, F.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Wong, C. T.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Vincent, A.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Godenschwege, T.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Boucrot, E.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Partridge, L.
Max Planck Institute for Biology of Ageing, Max Planck Society;

External Resource

(No access)

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

Citation

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.

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.