Key result
Heterogeneous erbb2 expression drives cardiomyocyte delamination and trabeculation via PI3K and Arp2/3 signaling.
Why the study?
The mechanisms governing cardiomyocyte fate decisions during myocardial wall development into trabeculae versus the compact layer remain unclear.
This study reveals that intrinsic variations in erbb2 expression drive cardiac trabeculation by promoting PI3K-Arp2/3-mediated actomyosin network remodeling and cell delamination.
No immediate clinical implications; extends zebrafish models of trabeculation but leaves open human relevance.
The myocardial wall arises from a single layer of cardiomyocytes, some delaminate to create trabeculae while others remain in the compact layer. However, the mechanisms governing cardiomyocyte fate decisions remain unclear. Using single-cell RNA sequencing, genetically encoded biosensors, and in toto live imaging, we observe intrinsic variations in erbb2 expression and its association with trabecular fate. Specifically, erbb2 promotes PI3K activity and recruits the Arp2/3 complex, inducing a polarized accumulation of the actomyosin network to drive cell delamination. Subsequently, the lineage-committed nascent trabeculae trigger Notch activity in neighboring cardiomyocytes to suppress erbb2 expression and reduce cell tension, thereby confining them to the compact layer. Overall, this genetic and cellular interplay governs compact and trabecular cell fate determination to orchestrate myocardial pattern formation.
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Liang et al. (2025) studied Cardiac trabeculation and heart development. erbb2 manipulation (genetic and pharmacological) vs. Wild-type controls or DMSO was evaluated on Cardiomyocyte delamination and trabeculae formation.
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