Skip to main content
. Author manuscript; available in PMC: 2021 Mar 11.
Published in final edited form as: Cell Rep. 2021 Feb 16;34(7):108751. doi: 10.1016/j.celrep.2021.108751

Figure 5. Kmt2c deletion impairs IL-1β-driven myeloid differentiation and conveys a selective advantage to cycling, IL-1β-stimulated HSCs.

Figure 5.

(A–C) HSC, MPP, and HPC numbers in wild-type and Kmt2cΔ/Δ mice after treatment with PBS or IL-1β for 3 days. n = 8–9.

(D) CD45.2+ donor leukocyte chimerism in peripheral blood from primary recipients transplanted with 20 wild-type and Kmt2cΔ/Δ HSCs, after a 21-day treatment with vehicle (PBS) or IL-1β. n = 10–13.

(E) Phenotypic HSC subpopulations after IL-1β 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-1β 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).