Cargando…

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

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 ex...

Descripción completa

Detalles Bibliográficos
Autores principales: Ikeya, Tomoatsu, Broughton, Susan, Alic, Nazif, Grandison, Richard, Partridge, Linda
Formato: Texto
Lenguaje:English
Publicado: The Royal Society 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2817276/
https://www.ncbi.nlm.nih.gov/pubmed/19692410
http://dx.doi.org/10.1098/rspb.2009.0778
_version_ 1782177177874202624
author Ikeya, Tomoatsu
Broughton, Susan
Alic, Nazif
Grandison, Richard
Partridge, Linda
author_facet Ikeya, Tomoatsu
Broughton, Susan
Alic, Nazif
Grandison, Richard
Partridge, Linda
author_sort Ikeya, Tomoatsu
collection PubMed
description 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.
format Text
id pubmed-2817276
institution National Center for Biotechnology Information
language English
publishDate 2009
publisher The Royal Society
record_format MEDLINE/PubMed
spelling pubmed-28172762010-02-22 The endosymbiont Wolbachia increases insulin/IGF-like signalling in Drosophila Ikeya, Tomoatsu Broughton, Susan Alic, Nazif Grandison, Richard Partridge, Linda Proc Biol Sci Research articles 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. The Royal Society 2009-11-07 2009-08-19 /pmc/articles/PMC2817276/ /pubmed/19692410 http://dx.doi.org/10.1098/rspb.2009.0778 Text en © 2009 The Royal Society http://creativecommons.org/licenses/by/2.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research articles
Ikeya, Tomoatsu
Broughton, Susan
Alic, Nazif
Grandison, Richard
Partridge, Linda
The endosymbiont Wolbachia increases insulin/IGF-like signalling in Drosophila
title The endosymbiont Wolbachia increases insulin/IGF-like signalling in Drosophila
title_full The endosymbiont Wolbachia increases insulin/IGF-like signalling in Drosophila
title_fullStr The endosymbiont Wolbachia increases insulin/IGF-like signalling in Drosophila
title_full_unstemmed The endosymbiont Wolbachia increases insulin/IGF-like signalling in Drosophila
title_short The endosymbiont Wolbachia increases insulin/IGF-like signalling in Drosophila
title_sort endosymbiont wolbachia increases insulin/igf-like signalling in drosophila
topic Research articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2817276/
https://www.ncbi.nlm.nih.gov/pubmed/19692410
http://dx.doi.org/10.1098/rspb.2009.0778
work_keys_str_mv AT ikeyatomoatsu theendosymbiontwolbachiaincreasesinsulinigflikesignallingindrosophila
AT broughtonsusan theendosymbiontwolbachiaincreasesinsulinigflikesignallingindrosophila
AT alicnazif theendosymbiontwolbachiaincreasesinsulinigflikesignallingindrosophila
AT grandisonrichard theendosymbiontwolbachiaincreasesinsulinigflikesignallingindrosophila
AT partridgelinda theendosymbiontwolbachiaincreasesinsulinigflikesignallingindrosophila
AT ikeyatomoatsu endosymbiontwolbachiaincreasesinsulinigflikesignallingindrosophila
AT broughtonsusan endosymbiontwolbachiaincreasesinsulinigflikesignallingindrosophila
AT alicnazif endosymbiontwolbachiaincreasesinsulinigflikesignallingindrosophila
AT grandisonrichard endosymbiontwolbachiaincreasesinsulinigflikesignallingindrosophila
AT partridgelinda endosymbiontwolbachiaincreasesinsulinigflikesignallingindrosophila