Fig. 5

Depletion of platelets is also reflected in molecular signatures of LT-HSCs with different blood output. A UMAP plot representing the transcriptomic state of control and treated LT-HSC, MkP, and CFU-E (included cells with read count > 50,000, mitochondrial gene content < 10%); cell numbers in all 3 populations are included in Additional file 7: Table S4, and QC is included in Additional file 6: Fig. S3B-E. B Enriched processes in platelet-biased clones compared to control multipotent clones in platelet-depleted animals, shown are adjusted p values using the Benjamini–Hochberg multiple correction test (full list of processes Additional file 13: Table S7). C Itga2b expression in LSK CD150⁺48⁻eGFP⁺ cells measured 28 weeks + 10 days post-transplantation in vehicle-treated and platelet-depleted animals. D Increased mean fluorescence intensity (MFI) of Itga2b in LSK CD150 + 48-eGFP + in platelet depleted compared to vehicle-treated animals using Welch’s unequal variances t-test, p = 0.0073. E Volcano plot representing genes upregulated in newly emerged myeloid clones compared to PEB clones. F Gene overlap between platelet-depletion activated LT-HSC clones and clones activated in the serial transplantation in the study [18]. Differentially expressed genes were derived using the deseq2 R package. Pseudo-bulk samples were generated by adding gene expression matrices for cells belonging to active or low-output clones within one animal, which resulted in 4 samples (mice 5–8). These samples were used as input for deseq2