The foraging gene in Drosophila mediates metabolic as well as behavioral plasticity
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ABSTRACT: The foraging gene in Drosophila, encoding PKG, is known for its importance as a natural variant affecting behavioral plasticity. Here, we demonstrate that it also affects metabolic plasticity: Rovers show a greater response to changes in their food environment than do sitters. Using metabolic profiling, we define foraging- and food-dependent changes in metabolites indicating that Rover store energy predominantly as lipids, whereas sitter variants store it as carbohydrates, Such changes are reflected in gene expression patterns, indicating an influence of foraging on regulators of insulin signaling. Combining for alleles with mutants of positive insulin signaling regulators makes Rover responses sitter-like, but does not change sitter responses. Collectively these findings suggest that the effect on metabolic plasticity of foraging works through the insulin signaling pathway. Keywords: stress response, comparative genomic hybridization, genotype by environment Design: 3 genotypes x 2 treatments x 3 replicates. Treatments were leaving flies on lab food (control) or food-depriving them overnight with access to water. Three genotypes differed in foraging alleles: Rovers are homozygous for[R] (strain: BB), sitters homozygous for[s] (strain: ee, mutant sitters homozygous for[s2] (strain:s2) . Adult flies were 6-7 days post emergence. Three samples of equal numbers of male and females were collected per combination, frozen in liquid nitrogen, and heads were sieved for RNA extraction. This Gene by Environment design tests how presence or absence of food for a short period (overnight) affects gene expression in different foraging genotypes.
ORGANISM(S): Drosophila melanogaster
SUBMITTER: Clement Kent
PROVIDER: E-GEOD-14371 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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