Loss of unc45a precipitates arteriovenous shunting in the aortic arches.

Aortic arch malformations are common congenital disorders that are frequently of unknown etiology. To gain insight into the factors that guide branchial aortic arch development, we examined the process by which these vessels assemble in wild type zebrafish embryos and in kurzschluss(tr12) (kus(tr12)) mutants. In wild type embryos, each branchial aortic arch first appears as an island of angioblasts in the lateral pharyngeal mesoderm, then elaborates by angiogenesis to connect to the lateral dorsal aorta and ventral aorta.

Getting connected.

Establishing a network of blood vessels has been, for more reasons than one, an exciting field of research. In Development, Isogai et al. now describe in unprecedented resolution the dynamic process of angiogenesis in the trunk of the zebrafish embryo.

sonic hedgehog and vascular endothelial growth factor act upstream of the Notch pathway during arterial endothelial differentiation.

The appearance of molecular differences between arterial and venous endothelial cells before circulation suggests that genetic factors determine these cell types. We find that vascular endothelial growth factor (vegf) acts downstream of sonic hedgehog (shh) and upstream of the Notch pathway to determine arterial cell fate. Loss of Vegf or Shh results in loss of arterial identity, while exogenous expression of these factors causes ectopic expression of arterial markers.

Expression of a zebrafish Cathepsin L gene in anterior mesendoderm and hatching gland.

 During a differential display-based screen for developmentally regulated genes in zebrafish, we have isolated a cDNA for zebrafish cathepsin L, termed catL. The gene shows abundant expression in the anteriormost cells of the head process which give rise to the polster and later to the hatching gland. Expression of catL persists in these tissues until hatching.