PUBLICATION
Zebrafish small molecule screen in reprogramming/cell fate modulation
- Authors
- Yeh, J.R., and Munson, K.M.
- ID
- ZDB-PUB-100330-24
- 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.
Citation
Yeh, J.R., and Munson, K.M. (2010) Zebrafish small molecule screen in reprogramming/cell fate modulation. Methods in molecular biology (Clifton, N.J.). 636:317-327.
Abstract
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping