PUBLICATION

SCL/Tal-1 transcription factor acts downstream of cloche to specify hematopoietic and vascular progenitors in zebrafish

Authors
Liao, E.C., Paw, B.H., Oates, A.C., Pratt, S.J., Postlethwait, J.H., and Zon, L.I.
ID
ZDB-PUB-980415-5
Date
1998
Source
Genes & Development   12: 621-626 (Journal)
Registered Authors
Liao, Eric, Oates, Andrew, Paw, Barry, Postlethwait, John H., Pratt, Stephen J., Zon, Leonard I.
Keywords
clo; zebrafish; hematopoiesis; vasculogenesis
MeSH Terms
  • Hematopoietic Stem Cells/physiology*
  • Mutation
  • Proto-Oncogene Proteins*
  • Chromosome Mapping
  • Conserved Sequence
  • Gene Expression Regulation, Developmental
  • DNA-Binding Proteins/genetics*
  • DNA-Binding Proteins/metabolism
  • Embryo, Nonmammalian
  • Animals
  • Molecular Sequence Data
  • Amino Acid Sequence
  • Endothelium, Vascular/embryology*
  • Zebrafish Proteins*
  • Zebrafish/embryology*
  • Zebrafish/genetics*
  • Basic Helix-Loop-Helix Transcription Factors
  • Transcription Factors*
PubMed
9499398 Full text @ Genes & Dev.
Abstract
SCL/Tal-1 is a transcription factor necessary for hematopoietic stem cell differentiation. Although SCL is also expressed in endothelial and neural progenitors, SCL function in these cells remains unknown. In the zebrafish mutant cloche (clo), SCL expression is nearly abolished in hematopoietic and vascular tissues. Correspondingly, it was shown previously that clo fails to differentiate blood and angioblasts. Genetic analysis demonstrates that the clo mutation is not linked to the SCL locus. Forced expression of SCL in clo embryos rescues the blood and vascular defects, suggesting that SCL acts downstream of clo to specify hematopoietic and vascular differentiation.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping