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Updated: May 21, 2025

Identification and Analysis of Mouse Erythroid Progenitors using the CD71/TER119 Flow-cytometric Assay
Published on: August 5, 2011
In-depth functional analysis of BRD9 in fetal hematopoiesis reveals context-dependent roles
Yifan Zhang1,2, Masaki Nomura1,3,4, Koutarou Nishimura1,4
1Department of Hematology-Oncology, Institute of Biomedical Research and Innovation, Foundation for Biomedical Research and Innovation at Kobe, Kobe, Japan.
Abstract:
The hierarchical organization of hematopoietic stem cells (HSCs) governing adult hematopoiesis has been extensively investigated. However, the dynamic epigenomic transition from fetal to adult hematopoiesis remains incompletely understood, particularly regarding the involvement of epigenetic factors. In this study, we investigate the roles of BRD9, an essential component of the non-canonical BAF (ncBAF) complex known to govern the fate of adult HSCs, in fetal hematopoiesis. Consistent with observations in adult hematopoiesis, BRD9 loss impairs fetal HSC stemness and disturbs erythroid maturation. Intriguingly, the impact on myeloid lineage was discrepant: BRD9 loss inhibited and promoted myeloid differentiation in fetal and adult models, respectively. Through comprehensive transcriptomic and epigenomic analysis, we elucidate the differential roles of BRD9 in a context- and lineage-dependent manner. Our data uncover how BRD9/ncBAF complex modulates transcription in a stage-specific manner, providing deeper insights into the epigenetic regulation underlying the transition from fetal to adult hematopoiesis.
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