Fig. 7: LManVI-mediated communication between mitochondria and lysosomes may be a general event for some mitochondrial defect.
a Knockdown of dMrps23 in fly muscles dramatically decreased LManVI mRNA level. b, c Knockdown of LManVI in dMrps23 RNAi background aggravated the abnormal wing phenotypes (b) and further reduced ATP levels (c), while overexpression of HA-LManVI partially rescued these phenotypes. d Overexpression of HA-LManVI partially rescued the lifespan of dMrps23 RNAi flies. e LManVI transcription level was dramatically reduced in pink1B9 mutant flies. f Overexpression of HA-LManVI partially rescued the abnormal wing phenotypes of pink1B9 flies. g LManVI mRNA level was dramatically downregulated in S2 cells treated with Rot. h Overexpression of HA-LManVI partially restored ATP levels in Rot-treated S2 cells. All data were performed with three biological replicates (n = 3). For sample sizes: n = 10 fly thoraxes (a and e), 100 flies (b and f), or 6 fly thoraxes (c) were used in each replicate. For lifespan, sample sizes were shown in the figure (d). The error bars are mean ± SD. For the statistics, two-tailed unpaired t-test (a, e, and g), or one-way ANOVA with Tukey’s multiple comparisons test (b, c, f, and h) was used. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns means no significant difference. Data points indicate biological replicates. The plotted value on the column represents the mean of 3 biological replicates (b, c). Source data were provided as a Source Data file.
