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. 2018 Apr 17;26(1):162–178. doi: 10.1038/s41418-018-0108-5

Fig. 2.

Fig. 2

Disruption of the cisd-3.1 and cisd-3.2 gene functions lead to germline defects. a Representative images of one gonad arm in cisd-3.1(RNAi), cisd-3.2(RNAi), or cisd-3.1(RNAi); cisd-3.2(RNAi) in N2 wild-type or cisd-1(tm4993) 1-day old adult hermaphrodites. The RNAi control is when the respective genotype is fed HT115 bacteria with empty vector. The knock-down of the cisd-3.1 and/or cisd-3.2 gene function results in germline defects. Defects include abnormal oocyte number (left panel) and DTC migration (Mig) defects (right panel). The oocytes are outlined and the number of oocytes present in the gonad are represented. The dashed line indicates the DTC migration pattern and the black half-moon outlines the DTC. Scale bar = 20 μm. b There is a significant decrease in the number of maturing oocytes in the gonad arm of cisd-3.1(RNAi), cisd-3.2(RNAi) and cisd-3.1(RNAi); cisd-3.2(RNAi) animal relative to the respective control animal (N2 wild-type, black symbol or cisd-1(tm4993), gray symbol on scatter plot), (one-way ANOVA, Dunnett multiple comparison test, bar indicates P ≤ 0.05). c There is a significant increase in DTC migration defects in the cisd-3.1(RNAi), cisd-3.2(RNAi), and cisd-3.1(RNAi); cisd-3.2(RNAi) animal relative to N2 wild-type (one-way ANOVA, Dunnett multiple comparison test, bar indicates P < 0.05). For b and c, at least 30 animals from three independent experiments were examined; error bar equals standard deviation.