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Drosophila insulin-like peptide dilp1 increases lifespan and glucagon-like Akh expression epistatic to dilp2

Stephanie Post, Sifang Liao, Rochele Yamamoto, Jan A. Veenstra, Dick R. Nässel, Marc Tatar
doi: https://doi.org/10.1101/380410
Stephanie Post
1Department of Molecular Biology, Cell Biology and Biochemistry, Providence, RI, Brown University, United States of America.
2Department of Ecology and Evolutionary Biology, Providence, RI, Brown University, United States of America.
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Sifang Liao
3Department of Zoology, Stockholm University, S-10691 Stockholm, Sweden.
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Rochele Yamamoto
2Department of Ecology and Evolutionary Biology, Providence, RI, Brown University, United States of America.
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Jan A. Veenstra
4Institut de Neurosciences Cognitives et Intégratives d’Aquitaine (CNRS UMR5287), University of Bordeaux, Pessac, France.
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Dick R. Nässel
3Department of Zoology, Stockholm University, S-10691 Stockholm, Sweden.
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Marc Tatar
2Department of Ecology and Evolutionary Biology, Providence, RI, Brown University, United States of America.
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Summary

Insulin/IGF signaling (IIS) regulates essential processes including development, metabolism, and aging. The Drosophila genome encodes eight insulin/IGF-like peptide (dilp) paralogs, including tandem-encoded dilp1 and dilp2. Many reports show that longevity is increased by manipulations that decrease DILP2 in adults. In contrast, dilp1 is expressed primarily in pupal stages, but also during adult reproductive diapause, although we find that dilp1 is also highly expressed in adult dilp2 mutants under non-diapause conditions. The inverse expression of dilp1 and dilp2 suggests these genes interact to regulate aging. Here, we study dilp1 and dilp2 single and double mutants to describe epistatic and synergistic interactions affecting longevity, metabolism and adipokinetic hormone (AKH), a functional homolog of glucagon. Mutants of dilp2 extend lifespan and increase Akh mRNA and protein in a dilp1-dependent manner. Loss of dilp1 alone has no impact on these traits, whereas transgene expression of dilp1 increases lifespan in dilp1-dilp2 double mutants. On the other hand, dilp1 and dilp2 redundantly interact to control circulating sugar, starvation resistance and compensatory dilp5 expression. These later interactions do not correlate with patterns for how dilp1 and dilp2 affect longevity and AKH. Thus, repression or loss of dilp2 slows aging because its depletion induces dilp1, which acts as a pro-longevity factor. Likewise, dilp2 regulates Akh through epistatic interaction with dilp1. Akh and glycogen affect aging in C. elegans and Drosophila, suggesting that dilp2 modulates lifespan via dilp1 and in part by regulating Akh. Whether DILP1 acts as an insulin receptor agonist or inhibitor remains to be resolved.

Footnotes

  • sifang.liao{at}zoologi.su.se, rochele_yamamoto{at}brown.edu, jan-adrianus.veenstra{at}u-bordeaux.fr, dnassel{at}zoologi.su.se

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted July 30, 2018.
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Drosophila insulin-like peptide dilp1 increases lifespan and glucagon-like Akh expression epistatic to dilp2
Stephanie Post, Sifang Liao, Rochele Yamamoto, Jan A. Veenstra, Dick R. Nässel, Marc Tatar
bioRxiv 380410; doi: https://doi.org/10.1101/380410
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Drosophila insulin-like peptide dilp1 increases lifespan and glucagon-like Akh expression epistatic to dilp2
Stephanie Post, Sifang Liao, Rochele Yamamoto, Jan A. Veenstra, Dick R. Nässel, Marc Tatar
bioRxiv 380410; doi: https://doi.org/10.1101/380410

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