PUBLICATION

Oncostatin M and Kit-Ligand Control Hematopoietic Stem Cell Fate during Zebrafish Embryogenesis

Authors
Mahony, C.B., Pasche, C., Bertrand, J.Y.
ID
ZDB-PUB-180522-1
Date
2018
Source
Stem Cell Reports   10(6): 1920-1934 (Journal)
Registered Authors
Bertrand, Julien, Mahony, Christopher, Pasche, Corentin
Keywords
Kit-ligand, cKIT, hematopoietic niche, hematopoietic stem cells, oncostatin M, oncostatin M receptor (osmr), zebrafish
MeSH Terms
  • Animals
  • Biomarkers
  • Embryonic Development/drug effects*
  • Gene Expression
  • Hematopoietic Stem Cells/cytology*
  • Hematopoietic Stem Cells/drug effects
  • Hematopoietic Stem Cells/metabolism*
  • Immunohistochemistry
  • Lymphocytes/cytology
  • Lymphocytes/drug effects
  • Lymphocytes/metabolism
  • Models, Biological
  • Oncostatin M/pharmacology*
  • Oncostatin M Receptor beta Subunit/metabolism
  • Signal Transduction/drug effects
  • Stem Cell Factor/pharmacology*
  • Zebrafish*
PubMed
29779898 Full text @ Stem Cell Reports
Abstract
Understanding the molecular pathways controlling hematopoietic stem cell specification and expansion is a necessary milestone to perform regenerative medicine. Here, we used the zebrafish model to study the role of the ckit signaling pathway in this process. We show the importance of kitb/kitlgb signaling in the specification and expansion of hematopoietic stem cells (HSCs), in the hemogenic endothelium and caudal hematopoietic tissue (CHT), respectively. Moreover, we identified the zebrafish ortholog of Oncostatin M (osm) in the zebrafish genome. We show that the osm/osmr pathway acts upstream of kitb during specification of the hemogenic endothelium, while both pathways act synergistically to expand HSCs in the CHT. Moreover, we found that osm, in addition to its role in promoting HSC proliferation, inhibits HSC commitment to the lymphoid fate. Altogether, our data identified two cytokines, kitlgb and osm, secreted by the vascular niche, that control HSCs during early embryonic development.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping