Figure 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 2.

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Joslin Diabetes Center, United States; Harvard Medical School, United States; Boston University, United States
Figure 2.
Download figureOpen in new tabFigure 2. GSCs inhibit SKN-1 activity in the intestine.

(A) Representative images of SKN-1::green fluorescent protein (GFP) in intestinal nuclei; GFP channel (top), bright field (BF; bottom). (B) Accumulation of SKN-1::GFP in intestinal nuclei in GSC(−) animals. (C) skn-1-dependent activation of direct SKN-1 target genes (Robida-Stubbs et al., 2012) in response to GSC absence, detected by qRT-PCR. (D, E) Increased expression of gst-4p::GFP in the intestine of glp-1(ts) animals. Hypodermal gst-4p::GFP expression appeared to be unaffected. (D) Representative 10× images. (E) Intestinal gst-4p::GFP quantification. (FH) GSCs regulate SKN-1 parallel to DAF-16 and DAF-12. In (H), SKN-1 target genes are assayed by qRT-PCR. glp-1(ts) refers to glp-1(e2141ts), and horizontal black lines indicate strains lacking GSCs. (C, H) Data are represented as mean ± SEM. n = 3 for qRT-PCR samples. (B, EG) 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.07836.006