Figure 6—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 6—figure supplement 2.

Affiliation details

Joslin Diabetes Center, United States; Harvard Medical School, United States; Boston University, United States
Figure 6—figure supplement 2.
Download figureOpen in new tabFigure 6—figure supplement 2. SKN-1 is activated in response to FA signaling.

Accumulation of SKN-1 in intestinal nuclei in (A) response to arsenite exposure for 30 min or (B) daf-2 mutants is not impaired by sbp-1 RNAi. (C) Effects of OA and CO doses on intestinal gst-4p::GFP expression, compared to AS treatment. (D) Larval development and (E) egg laying rate are not affected by OA or CO treatment. CO supplementation induces intestinal (F) SKN-1 nuclear accumulation but not (G) DAF-16 accumulation. (H, I) DAF-16 accumulation in glp-1(e2141ts) is unaffected by sbp-1 RNAi. (H) Representative 40× DIC images of day-1 adults. (J) PMK-1 (p38 kinase) phosphorylation is not affected by GSC removal, consistent with a previous report (Alper et al., 2010). PMK-1 phosphorylation is increased dramatically by AS oxidative stress and reflects activation of its kinase activity (Inoue et al., 2005). (AC, F, G, I) GFP quantification with high, medium, low scoring. Numbers above bars denote sample size. p < 0.05*; p < 0.01**; p < 0.001***.

DOI: http://dx.doi.org/10.7554/eLife.07836.017