< Back to Article

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

Figure 7

Meta-analysis of 3 manipulations of the insulin/Tor signaling identifies rover-biased genes.

Three published studies decreased insulin/Tor effects via (A) ablation of dilp3 expressing cells [28], (B) overexpression of constitutively active foxo [29], or (C) rapamycin [30]. We used data from these papers to identify sets of genes in each study whose expression went up or down in response to the particular insulin/Tor manipulation (Table S6 gives full statistics and methods). For each gene set (expression up or down), we plot average log2 fold change between rovers and mutant sitters in our study on the vertical axis, one bar for FD flies and one for Fed flies. When gene expression is reduced by insulin signaling (e.g. increases due to dilp3/foxo/rapamycin ablation), food deprived rovers have significantly higher mean expression than sitters (far left in each panel). When gene expression is increased by insulin signaling (e.g. decreases due to dilp3/foxo/rapamycin ablation), fed rover expression is higher than sitters (far right each panel). This was true for gene sets used from the ablation of dilp3 expressing cells publication [28] (A), the overexpression of foxo publication [29] (B), and the rapamycin treatment paper [30] (C). This results in significant negative interactions (Table S6) for genes repressed by insulin signaling, and significant positive interactions for genes increased by insulin. Error bars = 1 s.e.m. Blue bars, mean rover expression is higher than sitter, red bars, mean sitter expression is higher than rover.

Figure 7