ZFIN ID: ZDB-PUB-070122-40
fgf1 is required for normal differentiation of erythrocytes in zebrafish primitive hematopoiesis
Songhet, P., Adzic, D., Reibe, S., and Rohr, K.B.
Date: 2007
Source: Developmental dynamics : an official publication of the American Association of Anatomists   236(3): 633-643 (Journal)
Registered Authors: Adzic, Dejan, Reibe, Saskia, Rohr, Klaus
Keywords: zebrafish, fibroblast growth factor 1, MDS, AML, hematopoiesis, gata1, ikaros
MeSH Terms:
  • Animals
  • Cell Differentiation/genetics
  • Cell Differentiation/physiology*
  • Erythrocytes/cytology
  • Erythrocytes/metabolism
  • Erythropoiesis*
  • Fibroblast Growth Factor 1/genetics
  • Fibroblast Growth Factor 1/physiology*
  • GATA1 Transcription Factor/genetics
  • GATA1 Transcription Factor/metabolism
  • Gene Expression Regulation, Developmental
  • Ikaros Transcription Factor/genetics
  • Ikaros Transcription Factor/metabolism
  • Phylogeny
  • Reverse Transcriptase Polymerase Chain Reaction
  • Zebrafish/embryology
  • Zebrafish/genetics*
  • Zebrafish/physiology
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed: 17219402 Full text @ Dev. Dyn.
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ABSTRACT
Hematopoiesis in vertebrate development involves an embryonic, primitive wave and a later, definitive wave in which embryonic blood cells are replaced with adult blood cells. We here show that zebrafish fgf1 is involved in vivo in primitive hematopoiesis. Fibroblast growth factor-1 (FGF1) morpholino knockdown leads to abnormal accumulation of blood cells in the posterior intermediate cell mass at 32 hr postfertilization. Expression of the erythroid markers gata1 and ika, normally diminishing in differentiating erythrocytes at this stage, is maintained at abnormally high levels in primitive blood cells. The onset of erythrocyte differentiation as assessed by o-dianisidine staining is severely delayed. Most fgf1 morphants later recover to wild-type appearance, and primitive erythrocytes eventually differentiate. Zebrafish fgf1 is syntenic to human FGF1, which maps to a critically deleted region in human del(5q) syndrome posing an increased risk of leukemia to patients. As its knockdown in zebrafish changes expression of gata1, a gene involved in hematopoietic stem cell decisions, FGF1 should be considered to play a role in the pathogenesis of del(5q) syndrome.
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