Runx1-deficient progenitors are impaired in their in vitro differentiation potential. (A) Two-dimensional box plots showing mean colony numbers obtained per 10³ sorted progenitors. Each progenitor type was evaluated in at least 2 biological replicates (independent sorts) performed in duplicate. Horizontal line, median; box, range; whiskers, ±SD. (B-C) Cytospins of dispersed cells from the indicated colonies and genotypes. Giemsa staining; original magnification ×20. Arrow in panel B indicates immature Ery progenitors and granulocytic forms. (D) Bar graph representing FACS data for expression of lineage markers on dispersed cells derived from colony assays of indicated progenitors and genotypes. Horizontal line, median; error bars, ±SD. (E-H) FACS analysis of dispersed cells from (E) GMP, (F) pre-GM, (G) XMP, and (H) MEP methylcellulose colonies confirming impaired myeloid differentiation and Meg-skewing of Runx1^Δ/Δ progenitors. (I) Thpo plasma level determined per mouse is depicted by a dot. Horizontal line, median; error bars, ±SE. (J) Bar graph representing FACS data for expression of lineage markers on dispersed cells derived from colony assays of indicated progenitors and genotypes. Horizontal line, median; error bars, ±SD. (K) Donor contribution in spleen in competitive transplantation experiment shows no impact of Runx1-deletion on myeloid contribution but a significant reduction in the contribution to Ery CD45⁺Ter119⁺ progenitors. (L) Representative FACS analysis for CD45 expression on cells within the Ery progenitor population (CD105⁺) in BM isolated from mice of the indicated genotype (n = 4 per cohort). P values for panels A, D, I, J, and K were calculated by an unpaired Student t test; **P < .05; ***P < .01.