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Fig. 5 | BMC Biology

Fig. 5

From: orsai, the Drosophila homolog of human ETFRF1, links lipid catabolism to growth control

Fig. 5

ETFRF1/LYRm5 rescues cellular and viability defects associated with osi knockdown. A Confocal microscopy images showing the progression of cell growth phenotypes in fat body cells expressing osiRNAi (GFP+, golden cells) that are growing among control fat body cells (GFP−). Images were taken every 24h until pupation. B Cell size defects are fully rescued upon expression of ETFRF1/LYRm5 or OsiSM. The graph shows the normalized area for GFP+ (active)/GFP− (inactive) fat body cells. Kruskal-Wallis test with Dunn’s multiple comparisons test was performed. Three fat bodies per genotype were analyzed, for each sample, data was normalized to the mean of the control (inactive cells) of the corresponding genotype, in order to independently compare the absolute value. Shapiro-Wilk test was used for normality assessment (see Additional file 2). Kruskal-Wallis with Dunn’s multiple comparisons test was used to determine significance. C–G Images were taken at 72h AEL. Left panels: Frequency distribution of fat body cells in which the flipase was inactive (grey bars) or active (colored bars) and thus activating expression of osiRNAi (C, the figure shown in panel A is included for direct comparison), osiSM (D), osiRNAi, osiSM (E), LYRm5 (F), or LYRm5, osiRNAi (G). The number of cells analyzed per genotype is included in the graph. Right panels: Representative images of fat body cells from individuals of the indicated genotypes. All photographs include phalloidin-rhodamine staining (purple) to mark cell outlines. Cells expressing the constructs of interest are labeled in gold. Bars represent 20 μm. The total number of samples analyzed is mentioned below the corresponding panel. All datasets and statistical analysis on which the conclusions are based are included in Additional file 2

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