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En Face Endocardial Cushion Preparation for Planar Morphogenesis Analysis in Mouse Embryos
Published on: July 27, 2022
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Distinct mechanisms regulate ventricular and atrial chamber wall formation.
Marga Albu1,2,3, Eileen Affolter1,2,3, Alessandra Gentile1,2,3,4
1Max Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.
Nature Communications
|September 17, 2024
Summary
Zebrafish atrial cardiomyocytes elongate and intercalate to form the heart's internal muscle network. This process, distinct from ventricular trabeculation, is regulated by Yap signaling.
Area of Science:
- Cardiovascular biology
- Developmental biology
- Cellular morphogenesis
Background:
- The heart's internal muscle structures are crucial for efficient contraction.
- Ventricular wall formation (trabeculation) involves cardiomyocyte delamination.
- Mechanisms of atrial wall formation remain poorly understood.
Purpose of the Study:
- To investigate the cellular and molecular mechanisms underlying atrial wall formation in zebrafish.
- To compare atrial muscle network formation with known ventricular trabeculation processes.
Main Methods:
- Longitudinal in vivo imaging of zebrafish embryos.
- Analysis of cardiomyocyte shape changes and tissue thickening.
- Investigated roles of Nrg/ErbB, Notch, and Yap signaling pathways.
Main Results:
- Observed that approximately 25% of atrial cardiomyocytes elongate along the heart's long axis.
- Elongation leads to cell intercalation and convergent thickening, forming the atrial muscle network.
- Found no evidence for Nrg/ErbB or Notch signaling in atrial muscle formation.
- Identified Yap signaling as a potential regulator of atrial cardiomyocyte elongation.
Conclusions:
- Atrial and ventricular internal muscle structures are built by distinct cellular and molecular mechanisms.
- Atrial muscle network formation relies on cardiomyocyte elongation and intercalation, regulated by Yap.
- This study reveals novel insights into cardiac morphogenesis and highlights pathway divergence between heart chambers.
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