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Multilineage priming of enhancer repertoires precedes commitment to the B and myeloid cell lineages in hematopoietic progenitors.

Authors
  • Em, Mercer
  • Yc, Lin
  • C, Benner
  • S, Jhunjhunwala
  • J, Dutkowski
  • M, Flores
  • M, Sigvardsson
  • Trey Ideker
  • Ck, Glass
  • C, Murre
Type
Published Article
Journal
Immunity
Publisher
Elsevier
Volume
35
Issue
3
Pages
413–425
Identifiers
DOI: 10.1016/j.immuni.2011.06.013
Source
Ideker Lab
License
Unknown

Abstract

Recent studies have documented genome-wide binding patterns of transcriptional regulators and their associated epigenetic marks in hematopoietic cell lineages. In order to determine how epigenetic marks are established and maintained during developmental progression, we have generated long-term cultures of hematopoietic progenitors by enforcing the expression of the E-protein antagonist Id2. Hematopoietic progenitors that express Id2 are multipotent and readily differentiate upon withdrawal of Id2 expression into committed B lineage cells, thus indicating a causative role for E2A (Tcf3) in promoting the B cell fate. Genome-wide analyses revealed that a substantial fraction of lymphoid and myeloid enhancers are premarked by the poised or active enhancer mark H3K4me1 in multipotent progenitors. Thus, in hematopoietic progenitors, multilineage priming of enhancer elements precedes commitment to the lymphoid or myeloid cell lineages.

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