Corrigendum: Iron overload is accompanied by mitochondrial and lysosomal dysfunction in WDR45 mutant cells (Brain (2018) 141 (3052-3064) DOI: 10.1093/brain/awy230)

Philip Seibler, Lena Burbulla, Marija Dulovic, Simone Zittel, Johanne Heine, Thomas Schmidt, Franziska Rudolph, Ana Westenberger, Aleksandar Rakovic, Alexander Munchau, Dimitri Krainc, Christine Klein

Research output: Contribution to journalComment/debate

Abstract

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.

Original languageEnglish (US)
Pages (from-to)E10
JournalBrain
Volume142
Issue number3
DOIs
StatePublished - Mar 1 2019

Fingerprint

Iron Overload
Osteogenesis Imperfecta
Ferritins
Brain
Data Display
Mutation
Dopaminergic Neurons
Movement Disorders
Missense Mutation
Nervous System Diseases
Neurodegenerative Diseases
Genes
Biomedical Research
Fibroblasts
Phenotype
alpha 2(I) collagen
corrigendum
Proteins

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Seibler, Philip ; Burbulla, Lena ; Dulovic, Marija ; Zittel, Simone ; Heine, Johanne ; Schmidt, Thomas ; Rudolph, Franziska ; Westenberger, Ana ; Rakovic, Aleksandar ; Munchau, Alexander ; Krainc, Dimitri ; Klein, Christine. / Corrigendum : Iron overload is accompanied by mitochondrial and lysosomal dysfunction in WDR45 mutant cells (Brain (2018) 141 (3052-3064) DOI: 10.1093/brain/awy230). In: Brain. 2019 ; Vol. 142, No. 3. pp. E10.
@article{444fb4eafda44eeca975699c55af662f,
title = "Corrigendum: Iron overload is accompanied by mitochondrial and lysosomal dysfunction in WDR45 mutant cells (Brain (2018) 141 (3052-3064) DOI: 10.1093/brain/awy230)",
abstract = "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.",
author = "Philip Seibler and Lena Burbulla and Marija Dulovic and Simone Zittel and Johanne Heine and Thomas Schmidt and Franziska Rudolph and Ana Westenberger and Aleksandar Rakovic and Alexander Munchau and Dimitri Krainc and Christine Klein",
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doi = "10.1093/brain/awy316",
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Seibler, P, Burbulla, L, Dulovic, M, Zittel, S, Heine, J, Schmidt, T, Rudolph, F, Westenberger, A, Rakovic, A, Munchau, A, Krainc, D & Klein, C 2019, 'Corrigendum: Iron overload is accompanied by mitochondrial and lysosomal dysfunction in WDR45 mutant cells (Brain (2018) 141 (3052-3064) DOI: 10.1093/brain/awy230)' Brain, vol. 142, no. 3, pp. E10. https://doi.org/10.1093/brain/awy316

Corrigendum : Iron overload is accompanied by mitochondrial and lysosomal dysfunction in WDR45 mutant cells (Brain (2018) 141 (3052-3064) DOI: 10.1093/brain/awy230). / Seibler, Philip; Burbulla, Lena; Dulovic, Marija; Zittel, Simone; Heine, Johanne; Schmidt, Thomas; Rudolph, Franziska; Westenberger, Ana; Rakovic, Aleksandar; Munchau, Alexander; Krainc, Dimitri; Klein, Christine.

In: Brain, Vol. 142, No. 3, 01.03.2019, p. E10.

Research output: Contribution to journalComment/debate

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

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.

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U2 - 10.1093/brain/awy316

DO - 10.1093/brain/awy316

M3 - Comment/debate

VL - 142

SP - E10

JO - Brain

JF - Brain

SN - 0006-8950

IS - 3

ER -