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Neuronal SKN-1B modulates nutritional signalling pathways and mitochondrial networks to control satiety

Fig 4

SKN-1B modulates TGF-β signalling and controls satiety.

A) Time spent in quiescence after fasting and re-feeding. Each bar represents a mean of 3 biological replicates, ± SEM, n>9 worms per group. B and C) Fluorescence expression pattern, 20x magnification (B), and levels (C), of Pdaf-7::GFP in ASIs responds to skn-1b mutation and food cues. In (C) each bar represents a mean of 3 biological replicates ± st. dev., n>230 worms per group. NS difference was found between WT samples in fasted vs re-fed conditions and NS difference was found between skn-1b samples at any point. This regulation of daf-7 is unlikely to be direct as there is no SKN-1 binding site within 3Kb of its transcriptional start site. D) Quantification of exploration. Each bar is a mean of 5 biological replicates, n>44 worms per group ± st. dev. All trials shown in S8A–S8F Fig. E) Time spent in quiescence after fasting and re-feeding. Each bar represents a mean of 3 biological replicates, ± SEM, n>10 worms per group. For A, C, D and E: Two-tailed t-test *p<0.05, **p< 0.001, ***p<0.0001, NS not significant.

Fig 4

doi: https://doi.org/10.1371/journal.pgen.1009358.g004