Introducing an expanded CAG tract into the huntingtin gene causes a wide spectrum of ultrastructural defects in cultured human cells - Fig 5

Ultrastructure of mutant cells with a deletion (clone 8D, panels a–d) or with an ORF shift (clone 8H, panels e–h) in the huntingtin gene. (a), (e) An overview of the cells. (b) Mitochondria with narrow cristae; the arrowhead marks an autolysosome. (c) A well-developed Golgi complex (G). (d) Defective mitochondria with a light, transparent matrix (marked with double arrows). (f) Mitochondria with a dense matrix and swollen cristae, in contact with ER membranes, and autolysosomes (marked with an arrowhead). (g) Long membranes of the ER (ER) near the cell nucleus; the arrowhead marks a large lysosome. (h) Accumulation of lipid bodies (L) in the cytoplasm. Contacts of mitochondria with ER membranes are indicated with arrows. N: nucleus. Scale bars: 1 μm.