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Notch1 acts via Foxc2 to promote definitive hematopoiesis via effects on hemogenic endothelium

Il Ho Jang1, Yi-Fen Lu2, Long Zhao3

  • 1Stem Cell Program and Division of Hematology/Oncology, Children's Hospital Boston and Dana-Farber Cancer Institute, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA; Stem Cell Transplantation Program, Manton Center for Orphan Disease Research, Children's Hospital Boston, Boston, MA; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA; Harvard Stem Cell Institute, Boston, MA; Department of Physiology, School of Medicine, Pusan National University, Yangsan, Republic of Korea;

Blood
|January 15, 2015
PubMed

Hematopoietic and vascular development share many common features, including cell surface markers and sites of origin. Recent lineage-tracing studies have established that definitive hematopoietic stem and progenitor cells arise from vascular endothelial-cadherin(+) hemogenic endothelial cells of the aorta-gonad-mesonephros region, but the genetic programs underlying the specification of hemogenic endothelial cells remain poorly defined. Here, we discovered that Notch induction enhances hematopoietic potential and promotes the specification of hemogenic endothelium in differentiating cultures of mouse embryonic stem cells, and we identified Foxc2 as a highly upregulated transcript in the hemogenic endothelial population. Studies in zebrafish and mouse embryos revealed that Foxc2 and its orthologs are required for the proper development of definitive hematopoiesis and function downstream of Notch signaling in the hemogenic endothelium. These data establish a pathway linking Notch signaling to Foxc2 in hemogenic endothelial cells to promote definitive hematopoiesis.

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