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Nat Commun. 2019 Sep 11;10(1):4113. doi: 10.1038/s41467-019-12068-x.

Biomechanical signaling within the developing zebrafish heart attunes endocardial growth to myocardial chamber dimensions.

Author information

1
Institute of Biochemistry and Biology, Potsdam University, D-14476, Potsdam, Germany.
2
Institute of Molecular Biology, Hannover Medical School, D-30625, Hannover, Germany.
3
Institute of Science and Technology Austria, 3400, Klosterneuburg, Austria.
4
Department of Cell Biology, National Cerebral and Cardiovascular Center Research Institute, Osaka, 565-8565, Japan.
5
Institute of Cell Biology and Neuroscience, Department of Developmental Biology of Vertebrates, Goethe Universität Frankfurt am Main, 60438, Frankfurt am Main, Germany.
6
Max Planck Institute for Molecular Biomedicine, 48149, Münster, Germany.
7
Cells-in-Motion Cluster of Excellence (EXC 1003-CiM), University of Münster, 48149, Münster, Germany.
8
AMED-CREST. National Cerebral and Cardiovascular Center, Osaka, 565-8565, Japan.
9
Division of Biological Sciences, University of California, San Diego, La Jolla, CA, 92093, USA.
10
Institute of Biochemistry and Biology, Potsdam University, D-14476, Potsdam, Germany. salim.seyfried@uni-potsdam.de.
11
Institute of Molecular Biology, Hannover Medical School, D-30625, Hannover, Germany. salim.seyfried@uni-potsdam.de.

Abstract

Intra-organ communication guides morphogenetic processes that are essential for an organ to carry out complex physiological functions. In the heart, the growth of the myocardium is tightly coupled to that of the endocardium, a specialized endothelial tissue that lines its interior. Several molecular pathways have been implicated in the communication between these tissues including secreted factors, components of the extracellular matrix, or proteins involved in cell-cell communication. Yet, it is unknown how the growth of the endocardium is coordinated with that of the myocardium. Here, we show that an increased expansion of the myocardial atrial chamber volume generates higher junctional forces within endocardial cells. This leads to biomechanical signaling involving VE-cadherin, triggering nuclear localization of the Hippo pathway transcriptional regulator Yap1 and endocardial proliferation. Our work suggests that the growth of the endocardium results from myocardial chamber volume expansion and ends when the tension on the tissue is relaxed.

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