Fig. 2: Bt infection leads to mitochondria damage.
a Observations of the mitochondrial morphology of transgenic C. elegans SJ4143(zcIs17 [Pges-1::GFPmt]) fed without or with bre-5 RNAi. The images depicted are representative images of worms treated by each strain (triangle: mitochondria in the fusion state, showing tubular shape; star: mitochondria in the split state, showing punctate shape which represents mitochondria fragmentation (MF). The scan bars represent 20 μm. N = 3 independent experiments. b Transgenic worms were treated with each Bt strain after being subjected to bre-5 RNAi (resistant to toxin exposure) or empty vector. Count the percentage of worms with the mitochondria fragmentation phenotype after treatment in each condition. N = 3 independent experiments containing at least 50 worms each. c Analysis of the mitochondrial membrane potential (ΔΨm) by fluorescent dye stetramethyl rhodamine ethyl ester under each treatment for 4 h. The level of ΔΨm was determined by the fluorescence intensity of each worm. N = 3 independent experiments containing at least 20 worms. d The relative ratio of mtDNA /nDNA was investigated by real-time PCR. N = 3 independent experiments. e The relative AMP/ATP ratio was measured in each condition. In each experiment, worms were treated for 4 h. N = 3 independent experiments. FCCP: a protonophore can decrease mitochondrial membrane potential; mdivi-1: an efficient inhibitor that attenuates mitochondrial division. Data points represent the mean values of three independent replicates, error bars denote the SD in (b), (d), and (e). The whiskers represent the data range (minimum–maximum), and the box shows the 75th percentile, 25th percentile, and median in (c). The p-value was determined by a Student’s t-test (Welch’s correction for unequal variances), ***p < 0.001, **p < 0.01, *p < 0.05.
