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Figure 1 | Molecular Brain

Figure 1

From: Mitochondrial dysfunction associated with increased oxidative stress and α-synuclein accumulation in PARK2 iPSC-derived neurons and postmortem brain tissue

Figure 1

Generation of PARK2 iPSCs. (A) iPSCs derived from control and PARK2 subjects, embryoid bodies (EBs), neurospheres (NSs), and neurons. Left three rows: iPSCs from Control A (YA9), Control B (WD39), PA (PA9), and PB (PB2) were immunopositive for the pluripotency markers Oct4 (green) and Nanog (red). Right three rows: Differentiation of iPSCs into tyrosine hydroxylase (TH)-positive (red) neurons via EB and NS formation. Scale bars: Phase contrast, 400 μm; Nanog and Oct4 immunostaining, 100 μm; EBs, 25 μm; NSs, 50 μm; neurons, 10 μm. (B) Deletion of exons 2–4 in clones PA1, 9 and 22; and of exons 6 and 7 in clones PB1, 2, 18, and 20 was confirmed. (C) Exons 2–4 were deleted in human dermal fibroblasts (HDFs) from PA and in PA1 iPSC lines. Exons 6 and 7 were deleted in HDFs from PB and PB1 iPSC lines. (D) Copy number profiles of whole chromosomes in PARK2 HDFs and iPSCs were assessed by comparative genomic hybridization (CGH) microarray analysis; there was no evidence that genomic aberrations were introduced during the process of establishing PARK2 iPSCs.

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