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