SNCA and inborn mitochondrial metabolism disorder: Figure 4 shows representative images of the fruiting body morphology of α-synuclein-expressing strains. The α-synuclein wild type and point mutant strains produced thin, long stalks like the parental strain, while strains expressing the C-terminally truncated form produced sparse fruiting bodies which had shorter and thicker stalks reminiscent of mitochondrial disease strains. This result is consistent with reports that the truncated α-synuclein is more toxic to mammalian cells than the A53T point mutant or wild type forms of the protein [8,50,51,52].