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Journal Article

The endosymbiont Wolbachia increases insulin/IGF-like signalling in Drosophila

MPS-Authors

Ikeya,  T.
Max Planck Society;

Broughton,  S.
Max Planck Society;

Alic,  N.
Max Planck Society;

Grandison,  R.
Max Planck Society;

Partridge,  L.
Max Planck Society;

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Citation

Ikeya, T., Broughton, S., Alic, N., Grandison, R., & Partridge, L. (2009). The endosymbiont Wolbachia increases insulin/IGF-like signalling in Drosophila. Proc Biol Sci, 276(1674), 3799-807. doi:rspb.2009.0778 [pii] 10.1098/rspb.2009.0778.


Abstract
Insulin/IGF-like signalling (IIS) is an evolutionarily conserved pathway that has diverse functions in multi-cellular organisms. Mutations that reduce IIS can have pleiotropic effects on growth, development, metabolic homeostasis, fecundity, stress resistance and lifespan. IIS is also modified by extrinsic factors. For instance, in the fruitfly Drosophila melanogaster, both nutrition and stress can alter the activity of the pathway. Here, we test experimentally the hypothesis that a widespread endosymbiont of arthropods, Wolbachia pipientis, can alter the degree to which mutations in genes encoding IIS components affect IIS and its resultant phenotypes. Wolbachia infection, which is widespread in D. melanogaster in nature and has been estimated to infect 30 per cent of strains in the Bloomington stock centre, can affect broad aspects of insect physiology, particularly traits associated with reproduction. We measured a range of IIS-related phenotypes in flies ubiquitously mutant for IIS in the presence and absence of Wolbachia. We show that removal of Wolbachia further reduces IIS and hence enhances the mutant phenotypes, suggesting that Wolbachia normally acts to increase insulin signalling. This effect of Wolbachia infection on IIS could have an evolutionary explanation, and has some implications for studies of IIS in Drosophila and other organisms that harbour endosymbionts.