FB2026_03 , released September 17, 2026
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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--3807.
FlyBase ID
FBrf0208962
Publication Type
Research paper
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.
PubMed ID
PubMed Central ID
PMC2817276 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Proc. Biol. Sci.
    Title
    Proceedings. Biological sciences / The Royal Society.
    Publication Year
    1990-
    ISBN/ISSN
    0962-8452 1471-2954
    Data From Reference
    Alleles (4)
    Genes (5)
    Insertions (1)
    Transgenic Constructs (3)