Fig 1: Kmt2c deletion impairs IL-1ß-driven myeloid differentiation and conveys a selective advantage to cycling, IL-1ß-stimulated HSCs(A–C) HSC, MPP, and HPC numbers in wild-type and Kmt2c?/? mice after treatment with PBS or IL-1ß for 3 days. n = 8–9.(D) CD45.2+ donor leukocyte chimerism in peripheral blood from primary recipients transplanted with 20 wild-type and Kmt2c?/? HSCs, after a 21-day treatment with vehicle (PBS) or IL-1ß. n = 10–13.(E) Phenotypic HSC subpopulations after IL-1ß treatment based on EPCR and CD34 expression.(F) Percent of HSCs with Kmt2c deletions after one cycle of PBS or 5-FU, with or without concomitant IL-1ß or TNF. n = 6–20. Error bars reflect standard deviation.*p < 0.05, **p < 0.01, ***p < 0.001; comparisons were made by two-tailed Student’s t test or one-way ANOVA with Holm-Sidak post hoc test (multiple comparisons).