ZFIN ID: ZDB-PUB-110701-10
Smarcd3b and Gata5 promote a cardiac progenitor fate in the zebrafish embryo
Lou, X., Deshwar, A.R., Crump, J.G., and Scott, I.C.
Date: 2011
Source: Development (Cambridge, England)   138(15): 3113-23 (Journal)
Registered Authors: Crump, Gage DeKoeyer, Deshwar, Ashish, Lou, Xin, Scott, Ian
Keywords: none
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Cell Differentiation/physiology
  • Cells, Cultured
  • Fibroblast Growth Factors/metabolism
  • GATA Transcription Factors/genetics
  • GATA Transcription Factors/metabolism
  • GATA5 Transcription Factor/genetics
  • GATA5 Transcription Factor/metabolism*
  • Gene Expression Regulation, Developmental
  • Heart/embryology*
  • Myocardium/cytology*
  • Myocardium/metabolism
  • Signal Transduction/physiology
  • T-Box Domain Proteins/genetics
  • T-Box Domain Proteins/metabolism
  • Transcription Factors/genetics
  • Transcription Factors/metabolism*
  • Zebrafish/anatomy & histology
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 21715426 Full text @ Development
Development of the heart requires recruitment of cardiovascular progenitor cells (CPCs) to the future heart-forming region. CPCs are the building blocks of the heart, and have the potential to form all the major cardiac lineages. However, little is known regarding what regulates CPC fate and behavior. Activity of GATA4, SMARCD3 and TBX5  the 'cardiac BAF' (cBAF) complex, can promote myocardial differentiation in embryonic mouse mesoderm. Here, we exploit the advantages of the zebrafish embryo to gain mechanistic understanding of cBAF activity. Overexpression of smarcd3b and gata5 in zebrafish results in an enlarged heart, whereas combinatorial loss of cBAF components inhibits cardiac differentiation. In transplantation experiments, cBAF acts cell autonomously to promote cardiac fate. Remarkably, cells overexpressing cBAF migrate to the developing heart and differentiate as cardiomyocytes, endocardium and smooth muscle. This is observed even in host embryos that lack endoderm or cardiac mesoderm. Our results reveal an evolutionarily conserved role for cBAF activity in cardiac differentiation. Importantly, they demonstrate that Smarcd3b and Gata5 can induce a primitive, CPC-like state.