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Fig. 4 | BMC Biology

Fig. 4

From: The evolutionarily conserved ESRE stress response network is activated by ROS and mitochondrial damage

Fig. 4

The loss of UPRmt and MAPKmt pathways caused early activation of the ESRE reporter. a Fluorescent images of worms expressing 3XESRE::GFP reporter reared on E. coli expressing empty vector (EV), atfs-1(RNAi), pmk-3(RNAi), or pmk-3(RNAi); atfs-1(RNAi). Worms were treated with 50 μM rotenone or vehicle (DMSO). Images were taken at 6 h after treatment. See Fig. S12 in Additional File 1 for quantification. b Quantification of DHE fluorescence of N2 worms reared on E. coli expressing empty vector (EV) or pmk-3(RNAi); atfs-1(RNAi). Worms were treated with 50 μM rotenone for 10 h. Fold changes were normalized to EV on DMSO. c Fluorescent images of Peredox::GFP reporter reared on E. coli expressing EV, atfs-1(RNAi), or pmk-3(RNAi). d Fluorescent images of PINK-1::GFP reporter reared on E. coli expressing empty vector (EV), atfs-1(RNAi), or pmk-3(RNAi). e Quantification of GFP fluorescence of ESRE native reporters with intact (Phsp-16.1::GFP) or removed (Phsp-16.1(dd)::GFP) ESRE motifs. Worms were reared on E. coli expressing empty vector (EV), atfs-1(RNAi), spg-7(RNAi), or spg-7(RNAi); atfs-1(RNAi) for 2 days. GFP values were normalized to EV. Representative images are shown; three biological replicates with ~ 400 worms/replicate were analyzed. Error bars represent SEM. p values were determined from b Student’s t test or e one-way ANOVA followed by Dunnett’s test. NS not significant, *p < 0.05, **p < 0.01

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