作者: Kathleen Nevis , Pablo Obregon , Conor Walsh , Burcu Guner-Ataman , C. Geoffrey Burns
DOI: 10.1002/DVDY.23928
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摘要: Background: The mammalian outflow tract (OFT) and primitive right ventricle arise by accretion of newly differentiated cells to the arterial pole heart tube from multi-potent progenitor second field (SHF). While mounting evidence suggests that genetic pathways regulating SHF development are highly conserved in zebrafish, this topic remains an active area investigation. Results: Here, we extend previous observations demonstrating zebrafish tbx1 (van gogh, vgo) mutants show ventricular OFT defects consistent with a role SHF-mediated cardiogenesis. Surprisingly, reveal through double situ analyses transcripts excluded cardiac cardiomyocytes, suggesting non-autonomous development. Further, find diminutive vgo animals results 25% decrease cardiomyocyte number occurs subsequent stages. Lastly, report although progenitors specified absence Tbx1, they fail be maintained due compromised cell proliferation. Conclusions: These studies highlight conservation Tbx1 function biology. Developmental Dynamics 242:540–549, 2013. © 2013 Wiley Periodicals, Inc.