Premium
Tbx1 is required for second heart field proliferation in zebrafish
Author(s) -
Nevis Kathleen,
Obregon Pablo,
Walsh Conor,
GunerAtaman Burcu,
Burns C. Geoffrey,
Burns Caroline E.
Publication year - 2013
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.23928
Subject(s) - zebrafish , tbx1 , biology , ventricle , progenitor cell , progenitor , microbiology and biotechnology , heart development , stem cell , genetics , medicine , promoter , gene , embryonic stem cell , gene expression
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 ventricular and OFT 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 and differentiated cardiomyocytes, suggesting a non‐autonomous role in SHF development. Further, we find that the diminutive ventricle in vgo animals results from a 25% decrease in cardiomyocyte number that occurs subsequent 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. Conclusions: These studies highlight conservation of Tbx1 function in zebrafish SHF biology. Developmental Dynamics 242:540–549, 2013 . © 2013 Wiley Periodicals, Inc.