PUBLICATION

tcf21+ epicardial cells adopt non-myocardial fates during zebrafish heart development and regeneration

Authors
Kikuchi, K., Gupta, V., Wang, J., Holdway, J.E., Wills, A.A., Fang, Y., and Poss, K.D.
ID
ZDB-PUB-110613-25
Date
2011
Source
Development (Cambridge, England)   138(14): 2895-902 (Journal)
Registered Authors
Fang, Yi, Gupta, Vikas, Holdway, Jennifer, Kikuchi, Kazu, Poss, Kenneth D., Wang, Jinhu, Wills, Airon
Keywords
heart regeneration, heart development, cardiomyocyte, epicardium, zebrafish, genetic fate-mapping
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Cell Differentiation/physiology
  • Cell Lineage/physiology
  • Fluorescent Antibody Technique
  • Gene Expression Regulation, Developmental/physiology*
  • Heart/embryology*
  • Morphogenesis/genetics
  • Morphogenesis/physiology*
  • Pericardium/cytology*
  • Pericardium/metabolism
  • Regeneration/genetics
  • Regeneration/physiology*
  • Transcription Factors/metabolism*
  • Zebrafish/embryology*
  • Zebrafish Proteins/metabolism*
PubMed
21653610 Full text @ Development
Abstract
Recent lineage-tracing studies have produced conflicting results about whether the epicardium is a source of cardiac muscle cells during heart development. Here, we examined the developmental potential of epicardial tissue in zebrafish during both embryonic development and injury-induced heart regeneration. We found that upstream sequences of the transcription factor gene tcf21 activated robust, epicardium-specific expression throughout development and regeneration. Cre recombinase-based, genetic fate-mapping of larval or adult tcf21+ cells revealed contributions to perivascular cells, but not cardiomyocytes, during each form of cardiogenesis. Our findings indicate that natural epicardial fates are limited to non-myocardial cell types in zebrafish.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping