Cardiac progenitors of the splanchnic mesoderm (primary and secondary heart field), cardiac neural crest, and the proepicardium are the major embryonic contributors to chick heart development. Their contribution to cardiac development occurs with precise timing and regulation during such processes as primary heart tube fusion, cardiac looping and accretion, cardiac septation, and the development of the coronary vasculature. Heart development is even more complex if one follows the development of the cardiac innervation, cardiac pacemaking and conduction system, endocardial cushions, valves, and even the importance of apoptosis for proper cardiac formation. This review is meant to provide a reference guide (Table 1) on the developmental timing according to the staging of Hamburger and Hamilton (1951) (HH) of these important topics in heart development for those individuals new to a chick heart research laboratory. Even individuals outside of the heart field, who are working on a gene that is also expressed in the heart, will gain information on what to look for during chick heart development. This reference guide provides complete and easy reference to the stages involved in heart development, as well as a global perspective of how these cardiac developmental events overlap temporally and spatially, making it a good bench top companion to the many recently written in-depth cardiac reviews of the molecular aspects of cardiac development.

Lack of septation of the cardiac outflow tract (OFT) results in persistent truncus arteriosus (PTA), a form of congenital heart disease. The outflow myocardium expands through addition of cells originating from the pharyngeal mesoderm referred to as secondary/anterior heart field, whereas cardiac neural crest (CNC) cellderived mesenchyme condenses to form an aortopulmonary septum. We show for the first time that a mutation in Wnt5a in mice leads to PTA. We provide evidence that Wnt5a is expressed in the pharyngeal mesoderm adjacent to CNC cells in both mouse and chicken embryos and in the myocardial cell layer of the conotruncus at the time when CNC cells begin to form the aortopulmonary septum in mice. Although expression domains of secondary heart field markers are not altered in Wnt5a mutant embryos, the expression of CNC cell marker PlexinA2 is significantly reduced. Stimulation of CNC cells with Wnt5a protein elicits Ca 2ϩ transients, suggesting that CNC cells are capable of responding to Wnt5a. We propose a novel model in which Wnt5a produced in the OFT by cells originating from the pharyngeal mesoderm signals to adjacent CNC cells during formation of the aortopulmonary septum through a noncanonical pathway via localized intracellular increases in Ca

Vertebrate neural crest cells, derived from the neural folds, generate a variety of tissues, such as cartilage, ganglia, and cranial (intramembranous) bone. The chick homolog of the helix-loop-helix transcriptional regulator Id2 is expressed in cranial but not trunk neural folds and subsequently in some migrating cranial neural crest cells. Ectopic expression of Id2 with recombinant retroviruses converted ectodermal cells to a neural crest fate, demonstrating that proper regulation of Id2 is important for sustaining epidermal traits. In addition, overexpression of Id2 resulted in overgrowth and premature neurogenesis of the dorsal neural tube. These results suggest that Id2 may allocate ectodermal precursors into neural rather than epidermal lineages.