Figure 5. PAPLA1 deficiency does not increase fat storage nor affects lipid mobilization.

(a) PAPLA1 mutants store normal fat reserves and are able to mobilize them completely. Note the difference to the Akh^A and bmm¹ mutants. Lipid content was determined prior to starvation, after 24 h of starvation, and after complete starvation. Lipid levels were normalized to the protein levels at the given time point, and standardized to the relative lipid levels of control flies prior to starvation. (b) Consistent with normal body fat storage, expression of lipolysis (bmm, AkhR) and lipogenesis (mdy, Desat1, ACC, FASN1) genes in PAPLA1 mutants is normal. (c) Adulthood-specific ubiquitous knockdown of PAPLA1 driven by daughterless-GeneSwitch (da-GS) decreases fat storage. Note the contrast to the corresponding knockdown of lipolytic genes bmm and AkhR. (d) Adulthood-specific overexpression of wild type PAPLA1 reduces lipid levels, similarly as overexpression of lipolytic genes bmm and AkhR. (e) Adulthood-specific knockdown of PAPLA1 in the fat body driven by the FBI-26-GeneSwitch (FBI-26-GS) driver does not affect fat storage. Two independent RNAi lines were used. Note the contrast to the obesogenic effects of the corresponding knockdown of the lipolytic genes bmm and AkhR. (f) Adulthood-specific overexpression of PAPLA1 in the fat body considerably increases fat storage. Note the contrast to the lean phenotype triggered by overexpression of Akh or bmm. All panels: Two-tailed Student’s t–test: *P < 0.05; **P < 0.01; ***P < 0.001.