AML1/Runx1 rescues Notch1-null mutation-induced deficiency of para-aortic splanchnopleural hematopoiesis

Blood. 2006 Nov 15;108(10):3329-34. doi: 10.1182/blood-2006-04-019570. Epub 2006 Aug 3.

Abstract

The Notch1-RBP-Jkappa and the transcription factor Runx1 pathways have been independently shown to be indispensable for the establishment of definitive hematopoiesis. Importantly, expression of Runx1 is down-regulated in the para-aortic splanchnopleural (P-Sp) region of Notch1- and Rbpsuh-null mice. Here we demonstrate that Notch1 up-regulates Runx1 expression and that the defective hematopoietic potential of Notch1-null P-Sp cells is successfully rescued in the OP9 culture system by retroviral transfer of Runx1. We also show that Hes1, a known effector of Notch signaling, potentiates Runx1-mediated transactivation. Together with the recent findings in zebrafish, Runx1 is postulated to be a cardinal down-stream mediator of Notch signaling in hematopoietic development throughout vertebrates. Our findings also suggest that Notch signaling may modulate both expression and transcriptional activity of Runx1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Cells, Cultured
  • Core Binding Factor Alpha 2 Subunit / administration & dosage
  • Core Binding Factor Alpha 2 Subunit / genetics
  • Core Binding Factor Alpha 2 Subunit / pharmacology*
  • Embryo, Mammalian
  • Gene Expression Regulation, Developmental
  • Hematopoiesis
  • Humans
  • Mice
  • Mice, Mutant Strains
  • Receptor, Notch1 / deficiency*
  • Receptor, Notch1 / genetics
  • Receptor, Notch1 / physiology
  • Transduction, Genetic
  • Viscera / cytology

Substances

  • Core Binding Factor Alpha 2 Subunit
  • Notch1 protein, mouse
  • RUNX1 protein, human
  • Receptor, Notch1