TY - JOUR
T1 - Corrigendum
T2 - Iron overload is accompanied by mitochondrial and lysosomal dysfunction in WDR45 mutant cells (Brain (2018) 141 (3052-3064) DOI: 10.1093/brain/awy230)
AU - Seibler, Philip
AU - Burbulla, Lena F.
AU - Dulovic, Marija
AU - Zittel, Simone
AU - Heine, Johanne
AU - Schmidt, Thomas
AU - Rudolph, Franziska
AU - Westenberger, Ana
AU - Rakovic, Aleksandar
AU - Munchau, Alexander
AU - Krainc, Dimitri
AU - Klein, Christine
PY - 2019/3/1
Y1 - 2019/3/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85062559833&partnerID=8YFLogxK
UR - http://www.mendeley.com/research/corrigendum-iron-overload-accompanied-mitochondrial-lysosomal-dysfunction-wdr45-mutant-cells-brain-2
U2 - 10.1093/brain/awy316
DO - 10.1093/brain/awy316
M3 - Comments/Debates
C2 - 30561516
AN - SCOPUS:85062559833
SN - 0006-8950
VL - 142
SP - E10
JO - Brain
JF - Brain
IS - 3
ER -