Skip to main content
. Author manuscript; available in PMC: 2016 Dec 27.
Published in final edited form as: Nat Chem Biol. 2016 Jun 27;12(8):641–647. doi: 10.1038/nchembio.2113

Figure 2. Tafazzin deficiency increases the glycerol turnover of CL in Drosophila and mammalian cells.

Figure 2

(a) Drosophila strains were cultured for 9 days with D-[U-13C6]-glucose or unlabeled glucose as control. Lipids were analyzed by MS and spectra are displayed in centroid mode. 13C was incorporated into PE of the wild-type (WT) and the tafazzin deletion strain (ΔTAZ). 13C was incorporated into CL and MLCL of ΔTAZ but not WT, indicating a very slow CL turnover in the WT. (b) The fractional syntheses of CL and MLCL species were determined from the relative abundances of 13C0, 13C3,13C6 and 13C9 isotopomers following labeling with D-[U-13C6]-glucose for the indicated time periods. Tafazzin deficiency caused an increase in the fractional synthesis of CL species in Drosophila (P<0.04, 3 d; P<0.01, 9 d), mouse fibroblasts (P<0.001), and human lymphoblasts (P<0.0001). The fractional syntheses of CL and MLCL were similar. Data (means±s.e.m., N=3) were analyzed by t-test.