Quantitative trait locus mapping of gravitaxis behaviour in Drosophila melanogaster.

Drosophila melanogaster, like other organisms, move and orient themselves in response to the earth's gravitational force. The ability to sense and respond to gravity is essential for an organism to navigate and thrive in its environment. The genes underlying this behaviour in Drosophila remain elusive. Using 88 recombinant inbred lines, we have identified four quantitative trait loci (QTLs) that contribute to adult gravitaxis (geotaxis) behaviour in Drosophila. Candidate genes of interest were selected from the QTLs of highest significance based on their function in chordotonal organ formation. Quantitative complementation tests with these candidate genes revealed a role for skittles in adult gravitaxis behaviour in D. melanogaster.

Genotype-by-diet interactions drive metabolic phenotype variation in Drosophila melanogaster.

The rising prevalence of complex disease suggests that alterations to the human environment are increasing the proportion of individuals who exceed a threshold of liability. This might be due either to a global shift in the population mean of underlying contributing traits, or to increased variance of such underlying endophenotypes (such as body weight). To contrast these quantitative genetic mechanisms with respect to weight gain, we have quantified the effect of dietary perturbation on metabolic traits in 146 inbred lines of Drosophila melanogaster and show that genotype-by-diet interactions are pervasive. For several metabolic traits, genotype-by-diet interactions account for far more variance (between 12 and 17%) than diet alone (1-2%), and in some cases have as large an effect as genetics alone (11-23%). Substantial dew point effects were also observed. Larval foraging behavior was found to be a quantitative trait exhibiting significant genetic variation for path length (P = 0.0004). Metabolic and fitness traits exhibited a complex correlation structure, and there was evidence of selection minimizing weight under laboratory conditions. In addition, a high fat diet significantly increases population variance in metabolic phenotypes, suggesting decreased robustness in the face of dietary perturbation. Changes in metabolic trait mean and variance in response to diet indicates that shifts in both population mean and variance in underlying traits could contribute to increases in complex disease.