Expression analyses and functional characterization of Epcr^hi and Epcr^lo HSCs revealed an inverse correlation with CD41 expressing HSC subsets. (A) Frequencies (left) and percentages (right) of Epcr^hi and Epcr^lo HSCs within the phenotypic HSC compartment in BM and spleen of the indicated genotypes (n = 7-12 mice). (B) Analysis of colonies grown from FACS-sorted single Epcr^hi and Epcr^lo HSCs in liquid culture showing the percentages of colonies containing Mk (CD41⁺), myeloid (CD16⁺), or mixed (Mk and myeloid, CD41⁺/CD16⁺) cells after 10 days of culture (n = 128 cells per cell type/genotype and n = 3 mice). (C) Competitive BM transplantation. Hematopoietic lineage contributions of GFP⁺ Epcr^hi and Epcr^lo HSCs in the PB of recipients. Peripheral blood counts (top row) and donor derived (percentage of GFP⁺) cells (bottom row; n = 6 mice per genotype). Spleen weights of Epcr^hi and Epcr^lo HSC transplant recipients at 24 weeks after transplantation are shown (top right; n = 6-8 mice per cell type and genotype). (D) In vivo lineage contribution of Epcr^hi and Epcr^lo HSCs to HSPCs in transplant-recipient mouse BM and spleen at 24 weeks after transplantation (n = 4-6 mice cell type and genotype). (E) Percentages of Epcr^hi and Epcr^lo HSCs within the GFP⁺ subset of BM cells in transplant recipients at 24 weeks after transplantation. Note that only recipients of Epcr^hi HSC transplants were analyzed, because, at 24 weeks, recipients of Epcr^lo HSCs did not show GFP⁺ engraftment. All data are means ± standard error of the mean. *P < .05; **P < .01; ***P < .001.