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PLoS Pathog. 2015 Mar 31;11(3):e1004777. doi: 10.1371/journal.ppat.1004777. eCollection 2015 Mar.

The impact of host diet on Wolbachia titer in Drosophila.

Author information

1
Department of Biological Sciences, Florida International University Modesto A. Maidique Campus, Miami, Florida, United States of America; Biomolecular Sciences Institute, Florida International University Modesto A. Maidique Campus, Miami, Florida, United States of America.
2
Molecular, Cell, and Developmental Biology, University of California Santa Cruz, Santa Cruz, California, United States of America.
3
Instituto Gulbenkian de Ciência, Oeiras, Portugal.
4
Biology Department, Albion College, Albion, Michigan, United States of America.

Abstract

While a number of studies have identified host factors that influence endosymbiont titer, little is known concerning environmental influences on titer. Here we examined nutrient impact on maternally transmitted Wolbachia endosymbionts in Drosophila. We demonstrate that Drosophila reared on sucrose- and yeast-enriched diets exhibit increased and reduced Wolbachia titers in oogenesis, respectively. The yeast-induced Wolbachia depletion is mediated in large part by the somatic TOR and insulin signaling pathways. Disrupting TORC1 with the small molecule rapamycin dramatically increases oocyte Wolbachia titer, whereas hyper-activating somatic TORC1 suppresses oocyte titer. Furthermore, genetic ablation of insulin-producing cells located in the Drosophila brain abolished the yeast impact on oocyte titer. Exposure to yeast-enriched diets altered Wolbachia nucleoid morphology in oogenesis. Furthermore, dietary yeast increased somatic Wolbachia titer overall, though not in the central nervous system. These findings highlight the interactions between Wolbachia and germline cells as strongly nutrient-sensitive, and implicate conserved host signaling pathways by which nutrients influence Wolbachia titer.

PMID:
25826386
PMCID:
PMC4380406
DOI:
10.1371/journal.ppat.1004777
[Indexed for MEDLINE]
Free PMC Article

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