Regulation of cardiomyocyte behavior in zebrafish trabeculation by Neuregulin 2a signaling

S. Javad Rasouli and Didier Y. R. Stainier ()
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S. Javad Rasouli: Max Planck Institute for Heart and Lung Research
Didier Y. R. Stainier: Max Planck Institute for Heart and Lung Research

Nature Communications, 2017, vol. 8, issue 1, 1-11

Abstract: Abstract Trabeculation is crucial for cardiac muscle growth in vertebrates. This process requires the Erbb2/4 ligand Neuregulin (Nrg), secreted by the endocardium, as well as blood flow/cardiac contractility. Here, we address two fundamental, yet unresolved, questions about cardiac trabeculation: why does it initially occur in the ventricle and not the atrium, and how is it modulated by blood flow/contractility. Using loss-of-function approaches, we first show that zebrafish Nrg2a is required for trabeculation, and using a protein-trap line, find that it is expressed in both cardiac chambers albeit with different spatiotemporal patterns. Through gain-of-function experiments, we show that atrial cardiomyocytes can also respond to Nrg2a signalling, suggesting that the cardiac jelly, which remains prominent in the atrium, represents a barrier to Erbb2/4 activation. Furthermore, we find that blood flow/contractility is required for Nrg2a expression, and that while non-contractile hearts fail to trabeculate, non-contractile cardiomyocytes are also competent to respond to Nrg2a/Erbb2 signalling.

Date: 2017
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DOI: 10.1038/ncomms15281

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