HSCs cannot support hematopoiesis in the absence of NF-Ya and various genes implicated in HSCs behavior are dysregulated in HSCs. (A) CD45.1+ recipients received a BM transplant from NF-Ya^+/++Mx-cre (control) and NF-Ya^fl/fl+Mx-cre (ko, all CD45.2⁺) mice together with 30% CD45.1⁺ NF-Ya wt competitor cells. The mice were treated with pIpC at day 0. The CD45.1-to-CD45.2 ratio of Gr-1⁺, B220⁺, and CD3⁺ PB-cell populations was determined and normalized to day 0 (n = 5 for all data points except for ko samples day 30, 50, and 70; n = 4). (B) Mice from panel A were killed, and the indicated BM subpopulations were analyzed for CD45.1 versus CD45.2 expression and are shown in a bar graph, control (gray) and ko (black). (C) DNA from BM, spleen, thymus, and PB of NF-Ya^+/++Mx cre (control) and NF-Ya^fl/fl+Mx cre (ko) mutant BM chimeras 10 weeks after pIpC treatment was subjected to quantitative PCR analysis that measured the amount of NF-Ya–null allele. Single data points and averages, including SDs, are shown.