FGF signalling specifies haematopoietic stem cells through its regulation of somitic Notch signalling

Yoonsung Lee, Jennifer E. Manegold, Albert D. Kim, Claire Pouget, David L. Stachura, Wilson K. Clements and David Traver ()
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Yoonsung Lee: University of California, San Diego
Jennifer E. Manegold: University of California, San Diego
Albert D. Kim: University of California, San Diego
Claire Pouget: University of California, San Diego
David L. Stachura: University of California, San Diego
Wilson K. Clements: University of California, San Diego
David Traver: University of California, San Diego

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract Haematopoietic stem cells (HSCs) derive from haemogenic endothelial cells of the primitive dorsal aorta (DA) during vertebrate embryogenesis. The molecular mechanisms governing this unique endothelial to haematopoietic transition remain unclear. Here, we demonstrate a novel requirement for fibroblast growth factor (FGF) signalling in HSC emergence. This requirement is non-cell-autonomous, and acts within the somite to bridge the Wnt and Notch signalling pathways. We previously demonstrated that Wnt16 regulates the somitic expression of two Notch ligands, deltaC (dlc) and deltaD (dld), whose combined function is required for HSC fate. How Wnt16 connects to Notch function has remained an open question. Our current studies demonstrate that FGF signalling, via FGF receptor 4 (Fgfr4), mediates a signal-transduction pathway between Wnt16 and Dlc, but not Dld, to regulate HSC specification. Our findings demonstrate that FGF signalling acts as a key molecular relay within the developmental HSC niche to instruct HSC fate.

Date: 2014
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DOI: 10.1038/ncomms6583

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