Fig. 1: Metabolic profile of human BM HSPCs and their downstream progenitors.

a, The experimental study design depicting the generated datasets and their respective figure numbers. Created with BioRender.com. b, A schematic summary of the metabolomics results per pathway in human HSPCs and progenitors. Quantification bar plots as mean ± standard deviation show raw intensity values per biological replicate. Paired samples are linked by grey lines. Differentially abundant metabolites are depicted as coloured dots in the scheme. n = 17. P-adjusted value after paired two-sided Student’s t-test or Wilcoxon test is shown. NS, not significant; ND, not detected. c, GSEA of metabolic pathways on RNA-seq of human HSPCs versus progenitors. n = 4. d, Pathway activity score estimated by decoupleR in HSPCs versus progenitors RNA-seq. Differentially activated pathways are shown (P < 0.05). e, A subnetwork representing the COSMOS mechanistic hypothesis of metabolic and transcriptomic regulation of choline pathway, based on HSPCs versus progenitors metabolomics and RNA-seq datasets. Each node represents a gene or metabolite. The border colour depicts the estimated activity by the model. The arrow shape corresponds to the type of regulation based on ground knowledge. The fill colour of elements shows their level of differential expression or abundance in our measured data. P-adjusted value; *P < 0.05, **P < 0.01, ***P < 0.001. In b and c, n indicates the number of biological replicates per condition. For b, ten independent experiments were performed. NAA, N-acetylaspartic acid; α-KG, alpha-ketoglutarate; PEP, 2-phosphoenolpyruvate; GSSG, glutathione disulfide.