Philip Seibler, Lena F. Burbulla, Marija Dulovic, Simone Zittel, Johanne Heine, Thomas Schmidt, Franziska Rudolph, Ana Westenberger, Aleksandar Rakovic, Alexander Münchau, Dimitri Krainc, Christine Klein. Iron overload is accompanied by mitochondrial and lysosomal dysfunction in WDR45 mutant cells. Brain 2018; 141: 3052–3064. doi:10.1093/brain/awy230.
The authors apologize for the incorrect description of an iPSC line in the paper.
Authentication analysis at Coriell Institute for Medical Research (Camden, New Jersey) revealed that the iPSC line named HFF [ctrl(2)] in the article was not derived from a control individual but from cells of a female patient with osteogenesis imperfecta (GM17602/GM17604), carrier of a heterozygous missense mutation (p.G700C; NM_000089) in the COL1A2 gene.
Differentiated dopaminergic neurons from ctrl(2) were examined for expression levels of WDR45 (Fig. 5C), protein levels of SOD2 (Fig. 5D), and protein levels of mitochondrial ferritin (Fig. 5F) as one of two control lines compared to WDR45-mutant lines.
For all three experiments, the presented data display strong phenotypes and highly comparable levels between the two control lines. Importantly, all three experiments are replicative analysis of results shown in WDR45-mutant fibroblasts compared to controls: decreased expression of WDR45 (Fig. 1E), increased levels of SOD2 (Fig. 3D), and decreased levels of mitochondrial ferritin (Fig. 3F). This confirms that the analysed data in Fig. 5 are not influenced by the COL1A2 mutation in the line ctrl(2). Furthermore, mutations in the COL1A2 gene have not been associated with neurodegenerative diseases and the symptoms of neurological movement disorders have not been described for osteogenesis imperfecta.
Therefore, the correction does not alter the interpretation of the results as discussed in the paper.