Figure 3

Expression of PGC-1α rescues ER morphology in PGC1α-KO mice, and increases the number of mitochondrial contacts with ER. (a) Electron micrographs of neuronal soma in the SNpc of PGC1α-KO, PGC1α Inj and WT mice. Black arrowheads indicate the presence of giant mitochondria with disorganized cristae. (b) ER cisternae are colored in light gray. The cell membrane at the border of the neuronal cytosol is outlined. Note that PGC1α-KO mice display a disorganized and fragmented ER. In WT and PGC1α Inj mice, normal ER stacks are observed. Scale bar: 1 μm. (c,d) Quantification of the median length of ER profiles and number of branch points per μm of ER. (e) Relative length distribution of the ER segments in individual neurons from WT, PGC1α-KO and PGC1α Inj mice. Note the overall fragmentation of the ER in neurons from PGC1α-KO mice. Statistical analysis for c-d: one-way ANOVA with Newman-Keuls post-hoc test; WT: n = 51 neurons; PGC1α-KO: n = 51 neurons; PGC1α Inj: n = 60 neurons (f) Percentage of mitochondria having membrane contacts with ER. Note that PGC-1α significant increases the proportion of mitochondria with ER contacts. Statistical analysis: one-way ANOVA with Newman-Keuls post-hoc test; WT: n = 79 neurons; PGC1α-KO: n = 89 neurons; PGC1α Inj: n = 113 neurons; *p < 0.05, **p < 0.001 and ***p < 0.001. Micrographs were obtained from 3 animals in each group.