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Distinct roles of Wnt/beta-catenin and Bmp signaling during early cardiogenesis

Item Type:Article
Title:Distinct roles of Wnt/beta-catenin and Bmp signaling during early cardiogenesis
Creators Name:Klaus, A. and Saga, Y. and Taketo, M.M. and Tzahor, E. and Birchmeier, W.
Abstract:Heart formation requires the coordinated recruitment of multiple cardiac progenitor cell populations derived from both the first and second heart fields. In this study, we have ablated the Bmp receptor 1a and the Wnt effector beta-catenin in the developing heart of mice by using MesP1-cre, which acts in early mesoderm progenitors that contribute to both first and second heart fields. Remarkably, the entire cardiac crescent and later the primitive ventricle were absent in MesP1-cre; BmpR1a(lox/lox) mutants. Although myocardial progenitor markers such as Nkx2-5 and Isl1 and the differentiation marker MLC2a were detected in the small, remaining cardiac field in these mutants, the first heart field markers, eHand and Tbx-5, were not expressed. We conclude from these results that Bmp receptor signaling is crucial for the specification of the first heart field. In MesP1-cre; beta-catenin(lox/lox) mutants, cardiac crescent formation, as well as first heart field markers, were not affected, although cardiac looping and right ventricle formation were blocked. Expression of Isl1 and Bmp4 in second heart field progenitors was strongly reduced. In contrast, in a gain-of-function mutation of beta-catenin using MesP1-cre, we revealed an expansion of Isl1 and Bmp4 expressing cells, although the heart tube was not formed. We conclude from these results that Wnt/beta-catenin signaling regulates second heart-field development, and that a precise amount and/or timing of Wnt/beta-catenin signaling is required for proper heart tube formation and cardiac looping.
Keywords:BmpR1a, First Heart Field, Heart Looping, Mesoderm Patterning, Second Heart Field, Animals, Zebrafish
Source:Proceedings of the National Academy of Sciences of the United States of America
ISSN:0027-8424
Publisher:National Academy of Sciences (U.S.A.)
Volume:104
Number:47
Page Range:18531-18536
Date:20 November 2007
Additional Information:Copyright (c) 2007 by The National Academy of Sciences
Official Publication:https://doi.org/10.1073/pnas.0703113104
PubMed:View item in PubMed

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