PUBLICATION

Tbx1 is required for second heart field proliferation in zebrafish

Authors
Nevis, K., Obregon, P., Walsh, C., Guner-Ataman, B., Burns, C.G., and Burns, C.E.
ID
ZDB-PUB-130131-11
Date
2013
Source
Developmental Dynamics : an official publication of the American Association of Anatomists   242(5): 540-549 (Journal)
Registered Authors
Keywords
tbx1, zebrafish, heart, second heart field, cardiac
MeSH Terms
  • Stem Cells/metabolism
  • Stem Cells/physiology
  • Animals, Genetically Modified
  • Heart/embryology*
  • Heart/physiology
  • Animals
  • Embryo, Nonmammalian
  • Myocytes, Cardiac/cytology
  • Myocytes, Cardiac/metabolism
  • Myocytes, Cardiac/physiology
  • Zebrafish*/embryology
  • Zebrafish*/genetics
  • Zebrafish*/metabolism
  • Cell Proliferation*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • Zebrafish Proteins/physiology
  • Gene Expression Regulation, Developmental
  • Heart Ventricles/cytology
  • Heart Ventricles/embryology
  • T-Box Domain Proteins/genetics
  • T-Box Domain Proteins/metabolism
  • T-Box Domain Proteins/physiology*
  • Cell Differentiation/genetics
(all 24)
PubMed
23335360 Full text @ Dev. Dyn.
Abstract

Background: The mammalian outflow tract (OFT) and primitive right ventricle arise by accretion of newly differentiated cells to the arterial pole of the heart tube from multi-potent progenitor cells of the second heart field (SHF). While mounting evidence suggests that the genetic pathways regulating SHF development are highly conserved in zebrafish, this topic remains an active area of investigation. Results: Here, we extend previous observations demonstrating that zebrafish tbx1 (van gogh, vgo) mutants show conotruncal defects consistent with a conserved role in SHF-mediated cardiogenesis. Surprisingly, we reveal through double in situ analyses that tbx1 transcripts are excluded from cardiac progenitor cells or differentiated cardiomyocytes, suggesting a non-autonomous role in SHF development. Further, we find that the diminuitive ventricle in vgo animals results from a 25% decrease in cardiomyocyte numbers that occurs subseqent to heart tube stages. Lastly, we report that although SHF progenitors are specified in the absence of Tbx1, they fail to be maintained due to compromised SHF progenitor cell proliferation. Conclusion: These studies highlight conservation of the Tbx1 program in zebrafish SHF biology.

Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
f1TgTransgenic Insertion
    f2TgTransgenic Insertion
      fb7TgTransgenic Insertion
        tm208
          Point Mutation
          tu285
            Point Mutation
            1 - 5 of 5
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            Human Disease / Model
            No data available
            Sequence Targeting Reagents
            No data available
            Fish
            Antibodies
            Orthology
            No data available
            Engineered Foreign Genes
            Marker Marker Type Name
            DsRed2EFGDsRed2
            GFPEFGGFP
            ZsYellowEFGZsYellow
            1 - 3 of 3
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            Mapping
            No data available