GSE118192
MOF directs erythroid fate during hematopoiesis via RUNX1-GFI1b feedforward control (ChIP-Seq)
The balance between self-renewal and differentiation of hematopoietic stem cells (HSCs) is orchestrated by the combinatorial function of transcription factors and epigenetic regulators. Here, we report that the H4K16 acetyl-transferase MOF regulates chromatin accessibility and hematopoietic gene expression during erythroid commitment. Mof expression is controlled via a transcriptional feedforward pathway involving Runx1 and Gfi1b, which is crucial for the erythroid lineage bias. Single-cell RNA-seq of HSCs revealed that Mof haploinsufficient mice accumulate an otherwise rare HSC subset, indicating impaired differentiation.We propose that an intricate transcription factor network ensures dynamic chromatin targeting by MOF, which defines an essential epigenetic node regulating HSC plasticity, identity and differentiation. We propose that an intricate transcription factor network ensures dynamic chromatin targeting by MOF, which defines an essential epigenetic node regulating HSC plasticity, identity and differentiation. We propose that an intricate transcription factor network ensures dynamic chromatin targeting by MOF, which defines an essential epigenetic node regulating HSC plasticity, identity and differentiation. We propose that an intricate transcription factor network ensures dynamic chromatin targeting by MOF, which defines an essential epigenetic node regulating HSC plasticity, identity and differentiation. Overall design: Examination of MOF, H4K16ac and GATA-1 Genome-wide occupancy.