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ZIRC
ZFIN ID: ZDB-PUB-090116-21
Zebrafish granulocyte colony-stimulating factor receptor signaling promotes myelopoiesis and myeloid cell migration
Liongue, C., Hall, C.J., O'Connell, B.A., Crosier, P., and Ward, A.C.
Date: 2009
Source: Blood 113(11): 2535-2546 (Journal)
Registered Authors: Crosier, Phil, Hall, Chris, Ward, Alister C.
Keywords: none
MeSH Terms:
  • Amino Acid Sequence
  • Animals
  • Animals, Genetically Modified
  • Cell Movement/genetics*
  • Embryo, Nonmammalian
  • Gene Expression Regulation, Developmental
  • Hematopoiesis/genetics
  • Molecular Sequence Data
  • Myeloid Cells/metabolism
  • Myeloid Cells/physiology*
  • Myeloid Progenitor Cells/metabolism
  • Myeloid Progenitor Cells/physiology
  • Myelopoiesis/genetics*
  • Phylogeny
  • Receptors, Granulocyte Colony-Stimulating Factor/genetics*
  • Receptors, Granulocyte Colony-Stimulating Factor/metabolism
  • Receptors, Granulocyte Colony-Stimulating Factor/physiology
  • Sequence Homology, Amino Acid
  • Signal Transduction/genetics
  • Zebrafish/embryology
  • Zebrafish/genetics*
  • Zebrafish/physiology
PubMed: 19139076 Full text @ Blood
FIGURES
ABSTRACT
Granulocyte colony-stimulating factor receptor (GCSFR) signaling participates in the production of neutrophilic granulocytes during normal hematopoietic development, with a particularly important role during emergency hematopoiesis. This study describes the characterization of the zebrafish gcsf and gcsfr genes, which showed broad conservation and similar regulation to their mammalian counterparts. Morpholino-mediated knockdown of gcsfr and overexpression of gcsf revealed the presence of an anterior population of myeloid cells during primitive hematopoiesis that were dependent on GCSF/GCSFR for their development and migration. This contrasted with a posterior domain that was largely independent of this pathway. Definitive myelopoiesis was also partially dependent on a functional GCSF/GCSFR pathway. Injection of bacterial lipopolysaccharide elicited significant induction of gcsf expression and emergency production of myeloid cells, which was abrogated by gcsfr knockdown. Collectively, these data demonstrate GCSF/GCSFR to be a conserved signaling system for facilitating the production of multiple myeloid cell lineages in both homeostatic and emergency conditions, as well as for early myeloid cell migration, establishing a useful experimental platform for further dissection of this pathway.
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