Institute of Neuroscience Seminar

David Traver

Department of Cellular and Molecular Medicine

University of California, San Diego

Host: Judith Eisen

 

“Development of the Zebrafish Hematopoietic System”

 

Thursday, October 1, 2009, 4:00pm

110 Willamette

 

A major goal of regenerative medicine is to instruct formation of multipotent, tissue-specific stem cells from pluripotent embryonic stem cells (ESCs) for cell replacement therapies.  Generation of hematopoietic stem cells (HSCs) from ESCs is not currently possible, however, necessitating a better understanding of how HSCs normally arise during embryonic development.  We previously showed that hematopoiesis occurs through four distinct waves during zebrafish development, with HSCs arising in the final wave in close association with the dorsal aorta.  Recent reports have suggested that murine HSCs derive from hemogenic endothelial cells (ECs) lining the aortic floor.  Additional in vitro studies have similarly suggested that the hematopoietic progeny of ESCs arise through endothelial intermediates.  Using a permanent lineage tracing strategy, we have demonstrated that all four waves of developmental hematopoiesis derive from shared endothelial precursors, including the first HSCs that are the lineal founders of the adult hematopoietic system.  Utilizing combinations of fluorescent reporter transgenes, we have isolated the stepwise intermediates as hemogenic endothelium transitions to nascent HSCs.  In addition, we have utilized the unique strengths of the zebrafish embryo to image directly the birth of HSCs from the ventral wall of the dorsal aorta.  The genesis of HSCs from hemogenic endothelium is absolutely dependent upon the Notch signaling pathway.  In efforts to identify the signaling elements genetically upstream of Notch signaling, we have identified Wnt16, a non-canonical ligand of the Wnt signaling pathway that is required for HSC specification.  Generation of HSCs in Wnt16 knock-down animals is rescued by enforced Notch expression, demonstrating that Wnt16 regulates HSC formation in a Notch-dependent manner.  Taken together, these studies have demonstrated directly that HSCs are born from aortic endothelium, and have begun to elucidate the genetic factors required to instruct HSC formation from mesodermal precursors. 

 

Requests for accommodations related to disability should be made by calling Peg Morrow at 346-5222