To promote longevity under heat stress shares yeast aging factors with progeny through a down-regulation of the diffusion barrier in the membranes between the mitotic cells.
Tissue-level coordination of cardiac progenitor cells in the early mouse embryo produces a temporal compartmentalization of differentiation and morphogenesis essential for heart tube formation.
Cardiac-specific overexpression of a recently discovered micropeptide, DWORF, enhances calcium cycling and contractility in the heart and rescues the heart failure phenotype of a genetic mouse model of dilated cardiomyopathy.
Heat-induced local unfolding allows Hsf1 to form trimers and bind to DNA, which depends on Hsf1 concentration and is promoted, not inhibited, by Hsp90.
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.
A panel of seven new mouse strains with chromosomal duplications is used to identify a minimal genetic region required in three copies to cause congenital heart defects typical of human Down syndrome.
The proteins Heart of Glass (HEG1) and Rasip1 are both essential for cardiovascular development; and directly bind to each other to guide Rasip1 to endothelial cell junctions to support vascular integrity.
Dynamic regulation of the heat shock response depends on a negative feedback loop in which Hsf1 activates expression of Hsp70 and Hsp70 specifically and directly represses Hsf1 transactivation.
