Fetal ME induction suppresses HSC/MPP proliferation during late gestation. (A) UMAP representing P0 LK cells, cluster identities, and annotation based on CITE-seq performed after fetal ME induction. (B) Cluster distributions from control and ME-expressing cohorts. (C) Myeloid identity scores for cells in MPP cluster 24, as calculated by quadratic programming. (D) MLL::ENL transgene expression in HSC cluster 17 based on n = 4 pseudoreplicates. ∗∗∗P < .001. (E) Percent of cells within HSC (c17), MPP (c24), and GMP (c7) clusters at indicated cell cycle phases based on single-cell gene expression. (F) EdU incorporation in E18 LSK and GMP cells. n = 8 mice for control and n = 6 mice for Tet-Off-ME samples, ∗P < .05 by 2-tailed Student t test. (G) Percent of P0 LSK cells in S/G2/M phase of the cell cycle. n = 4 per group, ∗P < .05 by 2-tailed Student t test. (H) Venn diagram indicating genes that are more highly expressed in HSC/MPP clusters after postnatal ME induction relative to fetal induction, and genes that are downregulated by ME at P0 after fetal induction. (I) Expression of a subset of genes from the overlap in panel H. ∗∗∗P < .001 based on Wilcoxon signed-rank test. Ctl, control; Eryth, erythroid; UMAP, uniform manifold approximation and projection.