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The Drosophila foraging Gene Mediates Adult Plasticity and Gene–Environment Interactions in Behaviour, Metabolites, and Gene Expression in Response to Food Deprivation

Figure 5

foraging GEI is due to plasticity differences: rovers respond more to food than sitters.

In each histogram, the horizontal axis is the measure RNS (relative nutrient sensitivity; Methods) of which genotype has larger response to food. Blue bars, rovers respond more (RNS>0); red bars, mutant sitters respond more. (A) Behavioural plasticity: RNS measured using 9 different food media (Table S1C). RNS>0 for 8 of 9 (89%) and RNS = −0.004 for the ninth. Student t for RNS≠0, t = 2.99, df = 8, p = 0.009. (B) Metabolite plasticity: RNS for compounds with a significant response to food. 84% of these had RNS>0. Chi-square contingency test χ2 = 65.3, df = 1, p = 6.3×10−16. (C) Gene expression plasticity: RNS for 1,000 genes with significant food response. Of these, 77% had RNS>0 (χ2 = 305.3,df = 1, p<2.2×10−16). (D) Functional group plasticity. RNS for 300 Gene Ontology groups with significant food response. In 77% of these RNS>0 (χ2 = 88.6,df = 1, p<2.2×10−16). Average mutant sitter change on food deprivation is about ½ of rover. For simplicity, only rover versus mutant sitter RNS values are shown. This is conservative; rover versus natural sitter gene and gene group RNS distributions were more biased in favour of rovers than the rover vs. mutant sitter (Kolmogorov-Smirnov test for genes, D = 0.236, p<2.2×10−16; for gene groups D = 0.233, p = 0.000022).

Figure 5