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Additional file 1: Contains supplementary figures and tables to give further detail to the methods and results section

Germon et al, (2022) Supplementary files, comprising: A.Supplementary Figures 1 and 2 as a single pdf file. B. Supplementary Table 1. C. Supplementary Table 2.

Additional file 8. Liver enzymes over the study period. A: ASAT, B: ALAT, C: GGT.

Additional file 1. Overview of visits during the study period. V = Visit; SC = Screening; BL = Baseline; FD = Fist Dose; M = Month; X = BDNF sapling and all endpoint variable measurements.

Supplemental material, sj-docx-1-msj-10.1177_13524585211060686 for Reduced expression of mitochondrial fumarate hydratase in progressive multiple sclerosis contributes to impaired in vitro mesenchymal stromal cell-mediated neuroprotection by Pamela Sarkar, Juliana Redondo, Kelly Hares, Steven Bailey, Anastasia Georgievskaya, Kate Heesom, Kevin C Kemp, Neil J Scolding and Claire M Rice in Multiple Sclerosis Journal

Additional file 3. Baseline characteristics of healthy control children.

Additional file 2. Modified Grand Total of EEG Score (GTE-Score).

Additional file 10. Concentration of FTY720P (A) and FTY720 (B) over the study period.

Additional file 6. Changes of clinical scores over time. Change is indicated by absolute numbers of scores, eg. BL 7 and change over time -1, 3, -6: score changed from 7 to 6,9 and 3 respectively within the given time period. Changes over time in all scales and patients were not different in the intervals before during and after treatment. VABS = Vineland Adaptive Behaviour Scale; RSSS = Rett Severity Scale; HAS = Hand Apraxia Scale; M = Month of Study.

Additional file 4. BDNF(A) and NfL (B) in HC plotted by age and gender. Data of patients aged >15 years are shaded.

Additional file 6: Figures S1 and S2. Supplementary figures detailing in Figure S1 the location of deletions in other reported direct RNAseq data and in Figure S2 the MS/MS spectra for the peptide unique to the furing cleavage site deletion variant.

Table S1. ST239 and USA300 loci in epistasis with mupirocin resistance. Figure S1. The mupR mutation reduces the toxicity of the S. aureus strain SH1000. Table S2. DNA sequence results for SH1000 and MY40. Figure S2. Agr activity is not affected by the mupR mutation. Figure S3. Full length SDS-PAGE gel with butanol-extracted PSMs. Table S5. Strains constructed and used in this study. (DOCX 571 kb)

Ae. aegypti-Mapped PIT Hits Used in Analysis for Fig. 3A. (PDF 14 kb)

Additional Materials Pertaining to Virus Discovery in Aag2 Cells. Additional data (Figure S1) and detailed Results, Discussion, Materials and Methods, and References related to the discovery of Phasi Charoen-like virus in Aag2 cells. (PDF 312Â kb)

Non-Aedes Insect Genes (Pertaining to Figs. 2 and 3). List of PIT hits matching known dipteran, but not Ae. aegypti, genes. Supercontig and chromosomal locations, and existing gene annotation (if any), are specified. (PDF 47 kb)

Homology of New Ae. Aegypti Annotation to Known Dipteran Genes. (PDF 64Â kb)

Published Proteomic and Transcriptomic Data Used in Analysis for Fig. 2B. (PDF 73 kb)

Complete TE Proteome Detected By PIT in Aag2 Cells. (PDF 93Â kb)

Complete TE Proteome Detected By PIT in Aag2 Cells. (PDF 93Â kb)

Homology of New Ae. Aegypti Annotation to Known Dipteran Genes. (PDF 64Â kb)

Additional Materials Pertaining to Virus Discovery in Aag2 Cells. Additional data (Figure S1) and detailed Results, Discussion, Materials and Methods, and References related to the discovery of Phasi Charoen-like virus in Aag2 cells. (PDF 312Â kb)

Retromer controls cellular homeostasis through regulating integral membrane protein sorting and transport and by controlling maturation of the endo-lysosomal network. Retromer dysfunction, which is linked to neurodegenerative disorders including Parkinson’s and Alzheimer’s diseases, manifests in complex cellular phenotypes, though the precise nature of this dysfunction, and its relation to neurodegeneration, remain unclear. Here, we perform an integrated multi-omics approach to provide precise insight into the impact of Retromer dysfunction on endo-lysosomal health and homeostasis within a human neuroglioma cell model. We quantify widespread changes to the lysosomal proteome, indicative of broad lysosomal dysfunction and inefficient autophagic lysosome reformation, coupled with a reconfigured cell surface proteome and secretome reflective of increased lysosomal exocytosis. Through this global proteomic approach and parallel transcriptomic analysis, we provide a holistic view of Retromer function in regulating lysosomal homeostasis and emphasise its role in neuroprotection.