Hematopoietic stem cell development requires transient Wnt/β-catenin activity

J Exp Med. 2012 Jul 30;209(8):1457-68. doi: 10.1084/jem.20120225. Epub 2012 Jul 16.

Abstract

Understanding how hematopoietic stem cells (HSCs) are generated and the signals that control this process is a crucial issue for regenerative medicine applications that require in vitro production of HSC. HSCs emerge during embryonic life from an endothelial-like cell population that resides in the aorta-gonad-mesonephros (AGM) region. We show here that β-catenin is nuclear and active in few endothelial nonhematopoietic cells closely associated with the emerging hematopoietic clusters of the embryonic aorta during mouse development. Importantly, Wnt/β-catenin activity is transiently required in the AGM to generate long-term HSCs and to produce hematopoietic cells in vitro from AGM endothelial precursors. Genetic deletion of β-catenin from the embryonic endothelium stage (using VE-cadherin-Cre recombinase), but not from embryonic hematopoietic cells (using Vav1-Cre), precludes progression of mutant cells toward the hematopoietic lineage; however, these mutant cells still contribute to the adult endothelium. Together, those findings indicate that Wnt/β-catenin activity is needed for the emergence but not the maintenance of HSCs in mouse embryos.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aorta / embryology
  • Aorta / growth & development
  • Aorta / metabolism
  • Cell Differentiation / physiology
  • Endothelial Cells / metabolism
  • Gonads / embryology
  • Gonads / growth & development
  • Gonads / metabolism
  • Hematopoietic Stem Cell Transplantation / methods
  • Hematopoietic Stem Cells / cytology*
  • Hematopoietic Stem Cells / metabolism*
  • Mesonephros / embryology
  • Mesonephros / growth & development
  • Mesonephros / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mutation / genetics
  • Wnt Proteins / genetics
  • Wnt Proteins / metabolism*
  • beta Catenin / genetics
  • beta Catenin / metabolism*

Substances

  • CTNNB1 protein, mouse
  • Wnt Proteins
  • beta Catenin