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. Author manuscript; available in PMC: 2021 Dec 1.
Published in final edited form as: Arch Toxicol. 2020 Aug 20;94(12):4007–4022. doi: 10.1007/s00204-020-02879-z

Fig. 8. Glutamatergic neuron-specific CncC signaling modulation of MeHg effects on eclosion.

Fig. 8

a, b Expression pattern of the Elav(III)-GAL4 and OK371-GAL4 drivers (ventral view). c, d Eclosion ability with OK371-GAL4 driven CncC overexpression (>CncC) and knockdown (>CncCRNAi) compared to control (>w1118). e, f Eclosion ability with OK371-GAL4 driven Keap1 knockdown (>Keap1RNAi) and overexpression (>Keap1) compared to control (>w1118) (c-f n = 3, 450 flies/genotype/treatment, mean ± s.d.m., Z-test, *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001). g Representative images of MeHg effects on IFM morphology with either no change (>w1118), knockdown (>Keap1RNAi), or overexpression (>Keap1) of Keap1 in glutamatergic neurons. Number of missing dorsoventral muscles (DVMs, indicated by white asterisks) and dorsal lateral muscles (DLMs, indicated by white arrows) in each thorax were quantified at indicated MeHg treatment (h-j n ≥ 20/genotype/treatment, mean ± s.d.m., Kruskal-Wallis test with Dunn’s post-hoc for multiple comparisons within same muscle group, p<0.05, significant differences indicated by different letter labels).