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A proteomic atlas of insulin signalling reveals tissue-specific mechanisms of longevity assurance

MPG-Autoren

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

Sehlke,  R.
Max Planck Institute for Biology of Ageing, Max Planck Society;

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

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

Nagaraj,  N.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Essers,  P.
Max Planck Institute for Biology of Ageing, Max Planck Society;

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

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

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

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

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

Alic,  N.
Max Planck Institute for Biology of Ageing, Max Planck Society;

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

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

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Zitation

Tain, L. S., Sehlke, R., Jain, C., Chokkalingam, M., Nagaraj, N., Essers, P., et al. (2017). A proteomic atlas of insulin signalling reveals tissue-specific mechanisms of longevity assurance. Mol Syst Biol, 13(9), 939. doi:10.15252/msb.20177663.


Zitierlink: http://hdl.handle.net/21.11116/0000-0001-5932-3
Zusammenfassung
Lowered activity of the insulin/IGF signalling (IIS) network can ameliorate the effects of ageing in laboratory animals and, possibly, humans. Although transcriptome remodelling in long-lived IIS mutants has been extensively documented, the causal mechanisms contributing to extended lifespan, particularly in specific tissues, remain unclear. We have characterized the proteomes of four key insulin-sensitive tissues in a long-lived Drosophila IIS mutant and control, and detected 44% of the predicted proteome (6,085 proteins). Expression of ribosome-associated proteins in the fat body was reduced in the mutant, with a corresponding, tissue-specific reduction in translation. Expression of mitochondrial electron transport chain proteins in fat body was increased, leading to increased respiration, which was necessary for IIS-mediated lifespan extension, and alone sufficient to mediate it. Proteasomal subunits showed altered expression in IIS mutant gut, and gut-specific over-expression of the RPN6 proteasomal subunit, was sufficient to increase proteasomal activity and extend lifespan, whilst inhibition of proteasome activity abolished IIS-mediated longevity. Our study thus uncovered strikingly tissue-specific responses of cellular processes to lowered IIS acting in concert to ameliorate ageing.