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Previous studies have shown that ZBP‐89 (Zfp148) plays a critical role in erythroid lineage development, with its loss at the embryonic stage causing lethal anemia and thrombocytopenia. Its role in adult hematopoiesis has not been described. We now show that conditional deletion of ZBP‐89 in adult mouse hematopoietic stem/progenitor cells (HSPC) causes anemia and thrombocytopenia that are transient in the steady state, but readily uncovered following chemically induced erythro/megakaryopoietic stress. Unexpectedly, stress induced by bone marrow transplantation of  ZBP89 −  /  −   HSPC also resulted in a myeloid‐to‐B lymphoid lineage switch in bone marrow recipients. The erythroid and myeloid/B lymphoid lineage anomalies in  ZBP89 −  /  −   HSPC are reproduced in vitro in the  ZBP‐89 ‐silenced multipotent hematopoietic cell line FDCP‐Mix A4, and are associated with the upregulation of  PU.1  and downregulation of  SCL/Tal1  and  GATA‐1  in ZBP89‐deficient cells. Chromatin immunoprecipitation and luciferase reporter assays show that ZBP‐89 is a direct repressor of  PU.1  and activator of  SCL/Tal1  and  GATA‐1 . These data identify an important role for ZBP‐89 in regulating stress hematopoiesis in adult mouse bone marrow. S tem  C ells   2014;32:791–801

Stress Hematopoiesis Is Regulated by the Krüppel‐Like Transcription Factor ZBP‐89