(A) IL-1β or G-CSF increase Fancc mRNA expression in myeloid progenitor cells from WT mice but not Irf8^–/– mice. Bone marrow from WT or Irf8^–/– mice was cultured under GMP conditions (enriched for CD34⁺ cells). Some cells were treated with IL-1β or G-CSF. Fancc and Fancf mRNA was quantified by real-time PCR. Statistically significant differences in expression with versus without differentiation are indicated by *P < 0.01 or **P < 0.01 and with versus without IRF8-knockout by ***P < 0.01. There was no significant difference between IL-1β versus G-CSF induced expression (P > 0.1). (B) IL-1β increases FANCC protein in WT but not Irf8^–/– myeloid progenitor cells. The cells were analyzed by Western blots serially probed with antibody to FANCC and tubulin (loading control). (C) IL-1β increases FANCC, FANCJ, and RAD51 in the chromatin-enriched cell fraction. Bone marrow CD34⁺ cells from WT mice were treated with IL-1β for 24 or 48 hours, and chromatin and soluble fractions were evaluated by Western blots serially probed with antibodies to FANCC, FANCJ, RAD51, and GAPDH (loading control). (D) IL-1β and retinoic acid increase Fancc mRNA expression in U937 myeloid leukemia cells. U937 cells were stably transfected with an IRF8 expression vector or control vector. Cells were treated with IL-1β or RA/DMF, and Fancc mRNA was quantified by real-time PCR. Statistically significant differences in expression with versus without differentiation are indicated by *P < 0.01 or **P < 0.01 and with versus without IRF8 overexpression by ^#P < 0.01, ^##P < 0.01, or ^###P < 0.01.