Abstract
The cardiac trabeculae are sheet-like structures extending from the myocardium that function to increase surface area. A lack of trabeculation causes embryonic lethality due to compromised cardiac function. To understand the cellular and molecular mechanisms of trabecular formation, we genetically labeled individual cardiomyocytes prior to trabeculation via the brainbow multicolor system and traced and analyzed the labeled cells during trabeculation by whole-embryo clearing and imaging. The clones derived from labeled single cells displayed four different geometric patterns that are derived from different patterns of oriented cell division (OCD) and migration. Of the four types of clones, the inner, transmural, and mixed clones contributed to trabecular cardiomyocytes. Further studies showed that perpendicular OCD is an extrinsic asymmetric cell division that putatively contributes to trabecular regional specification. Furthermore, N-Cadherin deletion in labeled clones disrupted the clonal patterns. In summary, our data demonstrate that OCD contributes to trabecular morphogenesis and specification.
Highlights
Trabeculae are sheet-like structures that extend from the myocardium into the heart lumen to increase surface area, facilitating nutrient and gas exchange (Sedmera and Thomas, 1996)
To determine whether oriented cell division (OCD) is an asymmetric cell division that contributes to differential specification between the compact and trabecular zones, we examined the distribution of mRNAs in the dividing cells and the resulting two daughter cells
To distinguish endocardial cells from cardiomyocytes, embryos were stained for the endothelial cell marker PECAM in the far-red channel and counter-stained with DAPI in the blue channel to identify the geometric location of each cell in the heart
Summary
Trabeculae are sheet-like structures that extend from the myocardium into the heart lumen to increase surface area, facilitating nutrient and gas exchange (Sedmera and Thomas, 1996). The trabeculae largely coalesce into the ventricular wall to thicken the compact myocardium. A lack of trabeculation causes embryonic lethality, whereas trabeculae failing to undergo compaction will result in left ventricular non-compaction (LVNC) cardiomyopathy (Breckenridge et al, 2007; Gassmann et al, 1995; Jenni et al, 1999; Pignatelli et al, 2003; Towbin et al, 2015; Weiford et al, 2004; Zhao et al, 2014). Half a million Americans suffer from compromised heart function due to LVNC (Finsterer, 2010). Despite the fundamental functions of trabeculation, the molecular and cellular mechanisms underlying this process are not fully understood
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