Hypoplastic left heart syndrome is reflected by reduced proliferative capacity of patient iPSC-derived cardiomyocytes and requires the activity of LRP2/APOB proteins, likely in conjunction with SHH and WNT signaling pathways.
Analysis of embryonic mouse diaphragm reveals muscle and nerve left–right asymmetries set by a Nodal-dependent genetic cascade, which imprints different molecular signatures to left and right motoneurons that shape their innervation pattern.
Left-right asymmetric rotation of the Drosophila hindgut is driven by "cell sliding," a novel cellular behavior induced by chiral cell deformation, in which cells change their position relative to subjacent neighbors as sliding directionally.
Genetic analyses demonstrate that Gdf3/Vg1 is a maternal effect gene required for robust Nodal signaling during different phases of embryogenesis including germ-layer formation, Kupffer's vesicle morphogenesis, and left-right patterning.
Transcription factors downstream of Hippo signaling control formation of the Left-Right Organizer by regulating major signaling pathways, expression of transcription factors and regulators of epigenetic programming involved in this process.
A precise sequence of left-right asymmetries, combined with mechanical constraints, is sufficient to drive the looped morphogenesis of the embryonic heart tube, with potential impact for congenital heart defects.