Fig. 7: HuD expression upon oxidative stress in vitro and in sporadic ALS patients.

A, B The graphs show quantitative analysis of HuD mRNA levels in control conditions or upon acute stress treatment with 0.5 mM sodium arsenite (ARS) for 1 h in FUS^WT iPSCs derived spinal MNs monocultures at day 12 (A) or FUS^WT iPSCs derived co-cultures at day 7 (B) (n = 4). C Cells as in (A) were pre-treated or not with α-amanitin before oxidative stress induction with ARS (n = 4). D–F The experiments shown in (A–C) were repeated with the WTSI-FUS^WT iPSC line (n = 3 in (D, E); n = 4 in (F)). In (A–F) ATP5O expression was used for normalization and the graphs show the average, standard deviation, and p-values from 3 or 4 replicates, each consisting of a batch of differentiated iPSCs. A, B, D, E: Student’s t-test, unpaired, two tails, p-values are indicated in the graphs. C, F: ordinary one-way ANOVA, p = 1.0 × 10⁻¹⁰ (C), p = 7.5 × 10⁻⁶ (F); relevant post hoc Tukey test p-values for multiple comparisons are indicated in the graphs. In all graphs, bars indicate the mean and standard deviation, (G) Violin plots showing the expression levels, reported as log-transformed FPKM values, of HuD, NRN1, and GAP43 in post-mortem sporadic ALS patients’ cortex samples¹⁵. The adjusted p-values obtained from differential expression analyses have been corrected for multiple comparisons via the Benjamini-Hochberg procedure. Box boundaries: first and third quartile (Q1 and Q3); central line of box: median; whisker boundaries: the smallest and largest values within 1.5 times the interquartile range from Q1 and Q3. Source data are provided as a Source Data file.