PUBLICATION

Snail modulates the assembly of fibronectin via alpha5 integrin for myocardial migration in zebrafish embryos

Authors
Qiao, L., Gao, H., Zhang, T., Jing, L., Xiao, C., Xiao, Y., Luo, N., Zhu, H., Meng, W., Xu, H., Mo, X.
ID
ZDB-PUB-140513-279
Date
2014
Source
Scientific Reports   4: 4470 (Journal)
Registered Authors
Mo, Xianming, Zhang, Ting
Keywords
none
MeSH Terms
  • Animals
  • Cell Movement/genetics
  • Embryo, Nonmammalian
  • Embryonic Development*
  • Fibronectins/genetics
  • Fibronectins/metabolism*
  • Heart/growth & development
  • Integrin alpha5/genetics
  • Integrin alpha5/metabolism*
  • Morphogenesis/genetics
  • Myocardium/cytology
  • Transcription Factors/antagonists & inhibitors
  • Transcription Factors/genetics*
  • Zebrafish
  • Zebrafish Proteins/antagonists & inhibitors
  • Zebrafish Proteins/genetics*
PubMed
24667151 Full text @ Sci. Rep.
Abstract
The Snail family member snail encodes a zinc finger-containing transcriptional factor that is involved in heart formation. Yet, little is known about how Snail regulates heart development. Here, we identified that one of the duplicated snail genes, snai1b, was expressed in the heart region of zebrafish embryos. Depletion of Snai1b function dramatically reduced expression of α5 integrin, disrupted Fibronectin layer in the heart region, especially at the midline, and prevented migration of cardiac precursors, resulting in defects in cardiac morphology and function in zebrafish embryos. Injection of α5β1 protein rescued the Fibronectin layer and then the myocardial precursor migration in snai1b knockdown embryos. The results provide the molecular mechanism how Snail controls the morphogenesis of heart during embryonic development.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping