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Published Erratum
. 2024 Jun 13;147(1):99.
doi: 10.1007/s00401-024-02748-4.

Correction to: Disruption of MAM integrity in mutant FUS oligodendroglial progenitors from hiPSCs

Yingli Zhu  1 , Thibaut Burg  2   3 , Katrien Neyrinck  4 , Tim Vervliet  5 , Fatemeharefeh Nami  4 , Ellen Vervoort  6   7 , Karan Ahuja  4   8 , Maria Livia Sassano  6   7 , Yoke Chin Chai  4 , Arun Kumar Tharkeshwar  2   3 , Jonathan De Smedt  4 , Haibo Hu  9 , Geert Bultynck  5 , Patrizia Agostinis  6   7 , Johannes V Swinnen  10 , Ludo Van Den Bosch  2   3 , Rodrigo Furtado Madeiro da Costa  4 , Catherine Verfaillie  4
Affiliations
Published Erratum

Correction to: Disruption of MAM integrity in mutant FUS oligodendroglial progenitors from hiPSCs

Yingli Zhu et al. Acta Neuropathol. .
No abstract available

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Figures

Fig. 5
Fig. 5
Dysregulated glycerophospholipid metabolism in mutant FUS iPSC-derived OPCs. a Scheme of joint-pathway analysis. b, f Volcano plots of upregulated (red) and downregulated (blue) genes in FUS-mutant OPCs, compared to isogenic controls. Genes with log2FC < − 1.0 and − log10(p) > 2.0 were considered downregulated and log2FC > 1.0 with − log10(p) > 2.0 were considered upregulated. c, g Important dysregulated lipid species (red circles) selected by fold-change analysis. Both upregulated (log2FC > 1.0) and downregulated (log2FC < − 1.0) features are plotted in a symmetrical way. d, h, e, i Joint-pathway analysis (MetaboAnalyst v.5.0) shows upregulated and downregulated metabolic pathways in FUS-mutant OPCs, compared to isogenic controls. Each circle signifies a distinct pathway, with its size and shade reflecting the pathway’s impact and statistical significance (red denotes the highest significance). j, k Bar graphs displaying the percentage of known genes targeted by FUS (j) or spliced by FUS (k) within the different lipid-metabolism-related KEGG pathways (based on studies [12, 33, 37, 45, 64, 83]. l, m Bar graphs indicating the number of lipid-metabolism-related dysregulated genes (DEGs) (l) and the number of lipid-metabolism-related dysregulated genes that can be regulated by FUS (m) across previously published datasets compared to FUS-mutant OPCs. These datasets include bulk RNAseq data of the spinal cord from symptomatic FUS+/+ mice overexpressing wild-type human FUS compared to wild-type mice [79], single nuclei RNAseq data of primary human motor cortex OPCs/oligodendroglia of C9orf72-ALS patients compared with control human brain [50] and bulk RNAseq data of sporadic ALS patient motor cortex compared to control non-ALS control individuals [91], as well as between the so-called motor cortex of a ‘ALS_glia’ subtype group (identified by enriched astroglia, microglia and oligodendroglia dysregulated genes, and this even if—according to the authors—there was no selective neuronal loss) versus motor cortex all other sporadic ALS patients. n Scheme of glycerophospholipid metabolism, in which circles indicate metabolites and arrows indicate the enzymatic reaction with the gene name encoding the enzyme. Altered lipid classes in FUS-mutant OPCs are highlighted in blue, and arrows indicate whether the gene is upregulated or downregulated based on RNAseq data. Genes targeted by FUS are highlighted in red, while genes spliced by FUS are underlined
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Erratum for

  • Disruption of MAM integrity in mutant FUS oligodendroglial progenitors from hiPSCs.
    Zhu Y, Burg T, Neyrinck K, Vervliet T, Nami F, Vervoort E, Ahuja K, Sassano ML, Chai YC, Tharkeshwar AK, De Smedt J, Hu H, Bultynck G, Agostinis P, Swinnen JV, Van Den Bosch L, da Costa RFM, Verfaillie C. Zhu Y, et al. Acta Neuropathol. 2024 Jan 3;147(1):6. doi: 10.1007/s00401-023-02666-x. Acta Neuropathol. 2024. PMID: 38170217 Free PMC article.

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