Figure 5—figure supplement 2. | Lipid-mediated regulation of SKN-1/Nrf in response to germ cell absence

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Lipid-mediated regulation of SKN-1/Nrf in response to germ cell absence

Figure 5—figure supplement 2.

Affiliation details

Joslin Diabetes Center, United States; Harvard Medical School, United States; Boston University, United States
Figure 5—figure supplement 2.
Download figureOpen in new tabFigure 5—figure supplement 2. Analysis of the intestinal lipid droplet marker DHS-3::GFP, and TAG levels.

skn-1 RNAi increases DHS-3::GFP intensity in both wild-type and GSC(−) animals, whereas sbp-1 RNAi decreases DHS-3::GFP intensity. (A) 10× slide-mounted DHS-3::GFP images. White arrows indicate intestine-specific expression. (B, C) COPAS Biosorter quantification of DHS-3::GFP in live day-1 adult worms. (B) Representative 10× inverted scope images of worms suspended in M9 buffer used for COPAS scoring. (C) Graph of mean DHS-3::GFP fluorescence, assayed by COPAS. Numbers above bars denote sample size. Asterisks directly above bars indicate p values relative to WT or RNAi control. Asterisks above black lines denote effect of RNAi in glp-1(ts) background. RNAi was started from egg stage, and animals were raised at 25°C. (D) TAG levels are significantly elevated in skn-1 mutants. Data are represented as mean ± SEM. p < 0.01**; p < 0.001***.

DOI: http://dx.doi.org/10.7554/eLife.07836.013