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ZFIN ID: ZDB-PUB-100330-24
Zebrafish small molecule screen in reprogramming/cell fate modulation
Yeh, J.R., and Munson, K.M.
Date: 2010
Source: Methods in molecular biology (Clifton, N.J.)   636: 317-327 (Chapter)
Registered Authors: Yeh, Jing-Ruey (Joanna)
Keywords: Chemical screen, Zebrafish, Hematopoiesis, AML, Leukemia, Reprogramming, Cell fate, In vivo, Erythroid, Myeloid
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Cell Lineage
  • Cellular Reprogramming*
  • Core Binding Factor Alpha 2 Subunit/genetics
  • Core Binding Factor Alpha 2 Subunit/metabolism
  • Female
  • Hematopoietic Stem Cells/cytology
  • Hematopoietic Stem Cells/physiology*
  • In Situ Hybridization/methods
  • Male
  • Oncogene Proteins, Fusion/genetics
  • Oncogene Proteins, Fusion/metabolism
  • Small Molecule Libraries*
  • Zebrafish*/anatomy & histology
  • Zebrafish*/embryology
PubMed: 20336532 Full text @ Meth. Mol. Biol.
Embryonic zebrafish have long been used for lineage-tracing studies. In zebrafish embryos, the cell fate identities can be determined by whole-mount in situ hybridization, or by visualization of live embryos if using fluorescent reporter lines. We use embryonic zebrafish to study the effects of a leukemic oncogene AML1-ETO on modulating hematopoietic cell fate. Induced expression of AML1-ETO is able to efficiently reprogram hematopoietic progenitor cells from erythroid to myeloid cell fate. Using the zebrafish model of AML1-ETO, we performed a chemical screen to identify small molecules that suppress the cell fate switch in the presence of AML1-ETO. The methods discussed herein may be broadly applicable for identifying small molecules that modulate other cell fate decisions.