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. 2018 May 10;9(5):555. doi: 10.1038/s41419-018-0619-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a, b RNAi knockdown of fission (drp-1 and fis-1) and fusion (fzo-1 and eat-3) components with solvent caused DA neurodegeneration at day 9 post-hatching. With metabolite exposure, RNAi treated with drp-1, fis-1, or fzo-1 animals did not exhibit enhanced DA neurotoxicity compared to the corresponding solvent control. In contrast, a combination of S. ven metabolite and RNAi targeting eat-3 resulted in significant resistance to neurotoxicity. The scale bar is 10 μm. These data are presented as mean ± S.E.M.; n = 30 animals per replicate, three independent replicates; one-way ANOVA with Tukey’s post hoc test for multiple comparisons. *P < 0.05, **P < 0.01. Representative images of the six anterior dopaminergic neurons are shown in (b), with degenerating or missing neurons marked by arrows and normal neurons indicated by arrowheads. c An RNAi-sensitive strain with GFP expression in DA neurons was crossed to drp-1(tm1108) mutant animals. Homozygosity was confirmed by PCR. Loss-of-function drp-1(tm1108) exacerbated DA neurotoxicity compared with GFP only solvent control at day 9 post-hatching. RNAi knockdown of eat-3 did not result in resistance of neurotoxicity as observed in Fig. 4a. Data are represented as mean ± S.E.M; n = 30 animals per replicate, three independent replicates; one-way ANOVA with Tukey’s post hoc test for multiple comparisons. *P < 0.05, *P < 0.0001. d eat-3 mRNA levels were measured by qRT-PCR in animals treated with solvent (EtAc), S. ven metabolite, drp-1 (RNAi), or eat-3 (RNAi). The animals treated with metabolite showed significant lower eat-3 mRNA levels than when drp-1 was depleted by RNAi. Data represented as mean ± S.E.M.; three replicates comprises at least 100 animals each; one-way ANOVA with Tukey’s post hoc test for multiple comparisons. ****P < 0.0001.