The gata1/pu.1 lineage fate paradigm varies between blood populations and is modulated by tif1γ

Rui Monteiro, Claire Pouget, Roger Patient*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

63 Citations (Scopus)


Lineage fate decisions underpin much of development as well as tissue homeostasis in the adult. A mechanistic paradigm for such decisions is the erythroid versus myeloid fate decision controlled by cross-antagonism between gata1 and pu.1 transcription factors. In this study, we have systematically tested this paradigm in blood-producing populations in zebrafish embryos, including the haematopoietic stem cells (HSCs), and found that it takes a different form in each population. In particular, gata1 activity varies from autostimulation to autorepression. In addition, we have added a third member to this regulatory kernel, tif1β 3 (transcription intermediate factor-1γ 3). We show that tif1β 3 modulates the erythroid versus myeloid fate outcomes from HSCs by differentially controlling the levels of gata1 and pu.1. By contrast, tif1γ 3 positively regulates both gata1 and pu.1 in primitive erythroid and prodefinitive erythromyeloid progenitors. We therefore conclude that the gata1/pu.1 paradigm for lineage decisions takes different forms in different cellular contexts and is modulated by tif1γ 3.

Original languageEnglish
Pages (from-to)1093-1103
Number of pages11
JournalEMBO Journal
Issue number6
Publication statusPublished - 16 Mar 2011


  • gata1
  • haematopoiesis
  • lineage fate decisions
  • pu.1
  • tif1γ

ASJC Scopus subject areas

  • Molecular Biology
  • General Biochemistry,Genetics and Molecular Biology
  • General Immunology and Microbiology
  • General Neuroscience


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