Loss of ErbB2 activity in zebrafish mutants resulted in a complete lack of cardiac trabeculae, decreased fractional shortening, and an absence of cardiomyocyte proliferation during trabeculation.
ErbB2 signaling cell-autonomously regulates cardiac trabeculation through directional cardiomyocyte migration and proliferation, which is essential for normal cardiac function and conduction in zebrafish.
Cardiac trabeculation is a crucial morphogenetic process by which clusters of ventricular cardiomyocytes extrude and expand into the cardiac jelly to form sheet-like projections. Although it has been suggested that cardiac trabeculae enhance cardiac contractility and intra-ventricular conduction, their exact function in heart development has not been directly addressed. We found that in zebrafish erbb2 mutants, which we show completely lack cardiac trabeculae, cardiac function is significantly compromised, with mutant hearts exhibiting decreased fractional shortening and an immature conduction pattern. To begin to elucidate the cellular mechanisms of ErbB2 function in cardiac trabeculation, we analyzed erbb2 mutant hearts more closely and found that loss of ErbB2 activity resulted in a complete absence of cardiomyocyte proliferation during trabeculation stages. In addition, based on data obtained from proliferation, lineage tracing and transplantation studies, we propose that cardiac trabeculation is initiated by directional cardiomyocyte migration rather than oriented cell division, and that ErbB2 cell-autonomously regulates this process.
Liu et al. (Tue,) conducted a other in Cardiac trabeculation in zebrafish. ErbB2 mutation (loss of ErbB2 activity) was evaluated on Cardiac function, fractional shortening, conduction pattern, and cardiomyocyte proliferation. Loss of ErbB2 activity in zebrafish mutants resulted in a complete lack of cardiac trabeculae, decreased fractional shortening, and an absence of cardiomyocyte proliferation during trabeculation.