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

Tain, L. S.; Sehlke, R.; Jain, C.; Chokkalingam, M.; Nagaraj, N.; Essers, P.; Rassner, M.; Gronke, S.; Froelich, J.; Dieterich, C.; Mann, M.; Alic, N.; Beyer, A.; Partridge, L.

doi:10.15252/msb.20177663

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

MPS-Authors

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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https://www.ncbi.nlm.nih.gov/pubmed/28916541
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Citation

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.

Cite as: https://hdl.handle.net/21.11116/0000-0001-5932-3

Abstract

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.