ASF1B potentiated IL-1–driven AML progression in a murine model of leukemia, and the absence of ASF1B attenuated the leukemia progression. (A) A schematic representation of a murine AML bone marrow transduction/transplantation model mimicking ASF1B overexpression. Lineage (Lin⁻)-depleted wild-type bone marrow cells were transduced with MSCV-IRES-mCherry or MSCV-IRES-ASF1B-mCherry and MSCV-IRES-MLL-ENL-GFP constructs. After 48 hours of transduction, 10 000 sorted mCherry⁺GFP⁺ cells and supporting cells were injected into lethally irradiated C57BL/6 recipients. After engraftment confirmation, recipient mice were treated with 0.25 μg IL-1β or vehicle and monitored daily. The recipient mice were euthanized when they appeared moribund or showed signs of sickness. (B) Kaplan-Meier survival curve of recipient mice. The log-rank test was used for statistical analysis. ∗P < .05 and ∗∗P < .01 (C) Immunophenotyping of Asf1b^+/+, Asf1b^+/−, and Asf1b^−/− mice representing different cell populations in the bone marrow. The distribution of stem and progenitor cells in the bone marrow of Asf1b^+/+, Asf1b^+/−, and Asf1b^−/− mice was measured by flow cytometry. (D) A schematic representation of a murine AML bone marrow transduction/transplantation model to study the effect of ASF1B deletion on leukemia progression. Lineage (Lin⁻)-depleted Asf1b^+/+, Asf1b^+/−, and Asf1b^−/− bone marrow cells were transduced with MSCV-IRES-MLL-ENL-GFP retrovirus. After 48 hours of transduction, 25 000 sorted Lin⁻GFP⁺ cells and supporting cells were injected into lethally irradiated C57BL/6 recipients. After engraftment confirmation, recipient mice were treated with 0.25 μg IL-1β or vehicle and monitored daily. (E) Kaplan-Meier survival curve of recipient mice. The log-rank test was used for statistical analysis. ∗∗P < .01.