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. Author manuscript; available in PMC: 2012 Nov 11.
Published in final edited form as: Cell. 2011 Oct 27;147(4):840–852. doi: 10.1016/j.cell.2011.09.045

Figure 3. Increased lipogenesis and SBP-1-dependent gene expression after sams-1 RNAi in C. elegans is linked to limited phosphatidylcholine (PC) production.

Figure 3

A. Schematic diagram of links between methyl production and phospholipid biosynthesis in nematodes. Enzymes whose functions are disrupted by RNAi in subsequent panels are shown in blue boxes. B. Analysis of metabolites in sams-1(RNAi) nematodes shows that PC precursors downstream of methylation steps are decreased (phosphocholine), whereas metabolites upstream (choline, ethanolamine, phosphoethanolamine) are unchanged or slightly increased. Error bars represent standard error between quadruplicate independent experiments. C. Quantitative analysis show that PC levels are diminished after sams-1(RNAi). Error bars represent standard error between quadruplicate independent experiments. D. GFP∷SBP-1 accumulates in intestinal nuclei after pcyt-1(RNAi). E. Quantitative measurement of pfat-7∷GFP intensity in C. elegans populations by a COPAS biosorter shows that RNAi knockdown of PC biosynthesis genes downstream of methylation steps activate this SBP-1-dependent reporter at similar levels to sams-1 RNAi. Blocking methylation-dependent PC production by interference with PMT-1 produces similar phenotypes to sams-1(RNAi), such as increased lipid droplet formation (F) and overexpression of SBP-1 transcriptional targets, fat-5 and fat-7 (G). Error bars show standard deviation, statistical relevance (p value) shown by <0.05, *; <0.01, **, <0.005, ***.