PUBLICATION

The AP-1 transcription factor component Fosl2 potentiates the rate of myocardial differentiation from the zebrafish second heart field

Authors
Jahangiri, L., Sharpe, M., Novikov, N., González-Rosa, J.M., Borikova, A., Nevis, K., Paffett-Lugassy, N., Zhao, L., Adams, M., Guner-Ataman, B., Burns, C.E., Burns, C.G.
ID
ZDB-PUB-160107-8
Date
2016
Source
Development (Cambridge, England)   143: 113-22 (Journal)
Registered Authors
Burns (Erter), Caroline, Burns, Geoff, Paffett-Lugassy, Noelle, Zhao, Long
Keywords
AP-1, Cardiac development, Fosl2, Heart, Second heart field, Zebrafish
MeSH Terms
  • Myocardium/cytology
  • Fos-Related Antigen-2/biosynthesis
  • Fos-Related Antigen-2/genetics
  • Fos-Related Antigen-2/metabolism*
  • Animals
  • Myocytes, Cardiac/cytology*
  • Amino Acid Sequence
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • Cell Differentiation/physiology*
  • Heart Defects, Congenital/genetics
  • Zebrafish/embryology*
  • Cell Proliferation/genetics
  • Gene Expression Regulation, Developmental
  • Animals, Genetically Modified
  • Transcription Factor AP-1/metabolism*
  • Heart/embryology*
  • Gene Knockout Techniques
  • Sequence Analysis, Protein
(all 19)
PubMed
26732840 Full text @ Development
Abstract
The vertebrate heart forms through successive phases of cardiomyocyte differentiation. Initially, cardiomyocytes derived from first heart field (FHF) progenitors assemble the linear heart tube. Thereafter, second heart field (SHF) progenitors differentiate into cardiomyocytes that are accreted to the poles of the heart tube over a well-defined developmental window. Although heart tube elongation deficiencies lead to life-threatening congenital heart defects, the variables controlling the initiation, rate and duration of myocardial accretion remain obscure. Here, we demonstrate that the AP-1 transcription factor, Fos-like antigen 2 (Fosl2), potentiates the rate of myocardial accretion from the zebrafish SHF. fosl2 mutants initiate accretion appropriately, but cardiomyocyte production is sluggish, resulting in a ventricular deficit coupled with an accumulation of SHF progenitors. Surprisingly, mutant embryos eventually correct the myocardial deficit by extending the accretion window. Overexpression of Fosl2 also compromises production of SHF-derived ventricular cardiomyocytes, a phenotype that is consistent with precocious depletion of the progenitor pool. Our data implicate Fosl2 in promoting the progenitor to cardiomyocyte transition and uncover the existence of regulatory mechanisms to ensure appropriate SHF-mediated cardiomyocyte contribution irrespective of embryonic stage.
Genes / Markers
Figures
Figure Gallery (14 images) / 2
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
No data available
Sequence Targeting Reagents
Target Reagent Reagent Type
fosl2MO1-fosl2MRPHLNO
fosl2TALEN1-fosl2TALEN
1 - 2 of 2
Show
Fish
Fish
f1Tg
f1Tg; fb7Tg
f1Tg + MO1-fosl2
f2Tg
fosl2fb15/fb15
fosl2fb15/fb15; f1Tg
fosl2fb15/fb15; f2Tg
fosl2fb16/fb16
fosl2fb16/fb16; f1Tg; fb7Tg
fosl2fb16/fb16; f2Tg
1 - 10 of 14
Show
Antibodies
Orthology
Gene Orthology
fosl2
1 - 1 of 1
Show
Engineered Foreign Genes
Marker Marker Type Name
AmCyanEFGAmCyan
DsRed2EFGDsRed2
GFPEFGGFP
KikGREFGKikGR
ZsYellowEFGZsYellow
1 - 5 of 5
Show
Mapping
No data available
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Citation
Jahangiri, L., Sharpe, M., Novikov, N., González-Rosa, J.M., Borikova, A., Nevis, K., Paffett-Lugassy, N., Zhao, L., Adams, M., Guner-Ataman, B., Burns, C.E., Burns, C.G. (2016) The AP-1 transcription factor component Fosl2 potentiates the rate of myocardial differentiation from the zebrafish second heart field. Development (Cambridge, England). 143:113-22.