Interestingly, males were more glycerol hypersensitive than female Drosophila. One possible explanation for this difference is that females are larger than the males and contain more water leading to suppression of glycerol hypersensitivity. Indirect evidence supporting glycerol hypersensitivity as a desiccation tolerance phenotype was obtained by the finding that yellow homozygous null mutant flies, previously shown to be desiccation sensitive using a starvation/desiccation assay were also glycerol hypersensitive. It should be noted that the function of the yellow protein, which is known to play a role in black melanin synthesis in the body cuticle, has not been fully elucidated. As mentioned previously, human glycerol kinase BAY-60-7550 expression is highest in the liver. Therefore, we used the c564-GAL4 driver which has previously been shown to drive expression of GAL4 in the larval fat body, a tissue that plays an important role in energy metabolism similar to that of mammalian liver. The c564-GAL4 driver has previously been used to drive RNAi expression in adult flies to explore gene function in relation to fat metabolism. However, it should be noted that in adult flies, the GAL4 expression pattern driven by c564-GAL4 is not fat body specific. Using a GFP reporter construct, GFP expression was observed to have a much wider expression pattern that included fat body, gut, malpighian tubules, salivary glands and eye. Therefore we speculate that glycerol hypersensitivity might not be due to decreased expression in the fat body alone. In addition to liver, mammalian glycerol kinase is also highly expressed in the kidney so the malpighian tubules, which perform a similar function to mammalian kidney, could be an important tissue for the glycerol hypersensitivity phenotype. Further RNAi experiments using additional GAL4 drivers might clarify which cell type/tissue is important for glycerol hypersensitivity. One advantage of using Drosophila as a model organism is the ability to perform genetic modifier screens. To this end, we used the glycerol hypersensitive phenotype to perform a preliminary screen of lethal transposon insertion mutants. Our aim was to show that our GKD Drosophila model could be used to identify genetic modifier loci. Conveniently, results of survivorship assays can be quantitatively analyzed, allowing lethal transposon insertion mutants to be ranked based on day of,50% Adriamycin survival and allows both suppressors and enhancers of glycerol hypersensitivity to be identified. The power of this type of screen increases with the number of lethal transposon insertion mutants screened and a full screen would be required to identify the best targets. Using an identical set of lethal transposon insertion mutants, data analysis of the preliminary glycerol hypersensitive survivorship screen revealed a much wider distribution of 50% survival times for dGyk-RNAi progeny compared to dGK-RNAi progeny.