[
Development & Evolution Meeting,
2008]
We have isolated a mutant strain with a greater than two-fold increase in fat accumulation compared to wild type. Genetic epistasis experiments indicate that the defect is not caused by a reduction in the activity of the insulin/insulin-like or TGF-beta signaling pathways but rather from a defect downstream of or in parallel to these pathways. We made extracts of fats from the mutants and analyzed them by gas chromatography. This analysis revealed that the fatty acids C16:1n9 and C18:1n9 were present at disproportionately higher levels than in wild type but that the fatty acid distribution was otherwise similar to that in wild type. Thus the mutant causes a global increase in fat accumulation as well as changes in the distribution of specific fatty acids. We have performed RNAi with a panel of 150 clones that have been shown to reduce fat in a wild-type background (1) and found 15 genes that can reduce fat in the background of the mutant. At the same time, we have performed QRT-PCR with 120 genes implicated in the fatty acid synthesis, beta-oxidation or other aspects of fat metabolism (2) and identified 25 genes whose expression is altered in the mutant. The expression and RNAi data are consistent with a model in which the increase in fat in the mutant is caused by increased expression of CPT-5, a carnitine palmitoyl transferase, and reduced expression of F52B11.2 and F08F8.1, which encode a phosphomannomutase and a novel protein respectively.