Distinct mechanisms regulate ventricular and atrial chamber wall formation

Marga Albu, Eileen Affolter, Alessandra Gentile, Yanli Xu, Khrievono Kikhi, Sarah Howard, Carsten Kuenne, Rashmi Priya, Felix Gunawan and Didier Y. R. Stainier ()
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Marga Albu: Department of Developmental Genetics
Eileen Affolter: Department of Developmental Genetics
Alessandra Gentile: Department of Developmental Genetics
Yanli Xu: Department of Developmental Genetics
Khrievono Kikhi: Partner Site Rhine-Main
Sarah Howard: Department of Developmental Genetics
Carsten Kuenne: Max Planck Institute for Heart and Lung Research
Rashmi Priya: Department of Developmental Genetics
Felix Gunawan: Department of Developmental Genetics
Didier Y. R. Stainier: Department of Developmental Genetics

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract Tissues undergo distinct morphogenetic processes to achieve similarly shaped structures. In the heart, cardiomyocytes in both the ventricle and atrium build internal structures for efficient contraction. Ventricular wall formation (trabeculation) is initiated by cardiomyocyte delamination. How cardiomyocytes build the atrial wall is poorly understood. Using longitudinal imaging in zebrafish, we found that at least 25% of the atrial cardiomyocytes elongate along the long axis of the heart. These cell shape changes result in cell intercalation and convergent thickening, leading to the formation of the internal muscle network. We tested factors important for ventricular trabeculation including Nrg/ErbB and Notch signaling and found no evidence for their role in atrial muscle network formation. Instead, our data suggest that atrial cardiomyocyte elongation is regulated by Yap, which has not been implicated in trabeculation. Altogether, these data indicate that distinct cellular and molecular mechanisms build the internal muscle structures in the atrium and ventricle.

Date: 2024
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DOI: 10.1038/s41467-024-52340-3

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