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. 2020 Oct 27;9:e56969. doi: 10.7554/eLife.56969

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© 2020, Ghosh et al

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Figure 3. — (A) BODIPY staining showing neutral lipid accumulation in the adipose tissue and oenocytes of control males (oeno^ts = oenocyte-Gal4^Gal80ts) and males with oenocyte-specific knockdown of ERK (oeno^ts>ERKi-1 and oeno^ts>ERKi-2) using two independent RNAi lines. (B) BODIPY staining showing neutral lipid accumulation in the adipose tissue and oenocytes of control males (oeno^ts) and males with oenocyte-specific over-expression of tsc1 and tsc2 (oeno^ts>tsc1,tsc2). (C) Mean lipid droplet size (≥10 microns in diameter) in the adipose tissue of flies shown in Figure 2A and B. Only oenocyte-specific loss of TOR signaling (oeno^ts>tsc1,tsc2) show a significant increase (p<0.001) compared to the control genotype. N = 6 animals, One-way ANOVA followed by Tukey’s HSD test, **** denotes p≤0.0001, error bars = SEM. (D) BODIPY staining showing neutral lipid accumulation in the adipose tissue and oenocytes of control males (oeno^ts) and males with oenocyte-specific over-expression of inr^DN (oeno^ts>inr^DN) and oenocyte-specific (oeno^ts>) knockdown of Pi3K92E (Dp110), Pi3K21B (Dp60) and akt1. (E) Mean lipid droplet size (≥10 microns in diameter) in the adipose tissue of flies shown in Figure 2D. Oenocyte-specific (oeno^ts>) knockdown of Pi3K92E (Dp110), Pi3K21B (Dp60), and akt1 lead to a significant increase (p<0.001 for Pi3K92E, and, p<0.0001 for Pi3K21B and akt1) compared to the control genotype. N = 6 animals, One-way ANOVA followed by Tukey’s HSD test, *** denotes p≤0.001, **** denotes p≤0.0001, error bars = SEM.

Figure 3—figure supplement 1. — (A) BODIPY staining showing neutral lipid accumulation in the adipose tissue and oenocytes of control males (oeno^ts = oenocyte-Gal4^Gal80ts) and males with oenocyte-specific knockdown of ERK (oeno^ts>ERKi-1 and oeno^ts>ERKi-2) using two independent RNAi lines. (B) BODIPY staining showing neutral lipid accumulation in the adipose tissue and oenocytes of control males (oeno^ts) and males with oenocyte-specific over-expression of tsc1 and tsc2 (oeno^ts>tsc1,tsc2). (C) Mean lipid droplet size (≥10 microns in diameter) in the adipose tissue of flies shown in Figure 2A and B. Only oenocyte-specific loss of TOR signaling (oeno^ts>tsc1,tsc2) show a significant increase (p<0.001) compared to the control genotype. N = 6 animals, One-way ANOVA followed by Tukey’s HSD test, **** denotes p≤0.0001, error bars = SEM. (D) BODIPY staining showing neutral lipid accumulation in the adipose tissue and oenocytes of control males (oeno^ts) and males with oenocyte-specific over-expression of inr^DN (oeno^ts>inr^DN) and oenocyte-specific (oeno^ts>) knockdown of Pi3K92E (Dp110), Pi3K21B (Dp60) and akt1. (E) Mean lipid droplet size (≥10 microns in diameter) in the adipose tissue of flies shown in Figure 2D. Oenocyte-specific (oeno^ts>) knockdown of Pi3K92E (Dp110), Pi3K21B (Dp60), and akt1 lead to a significant increase (p<0.001 for Pi3K92E, and, p<0.0001 for Pi3K21B and akt1) compared to the control genotype. N = 6 animals, One-way ANOVA followed by Tukey’s HSD test, *** denotes p≤0.001, **** denotes p≤0.0001, error bars = SEM.