Abstract
Fibronectin and its major receptor, integrin α5β1 are required for embryogenesis. These mutants have similar phenotypes, although, defects in integrin α5-deficient mice are milder. In this paper, we examined heart development in those mutants, in which the heart is formed, and discovered that both fibronectin and integrin α5 were required for cardiac morphogenesis, and in particular, for the formation of the cardiac outflow tract. We found that Isl1+ precursors are specified and migrate into the heart in fibronectin- or integrin α5-mutant embryos, however, the hearts in these mutants are of aberrant shape, and the cardiac outflow tracts are short and malformed. We show that these defects are likely due to the requirement for cell adhesion to fibronectin for proliferation of myocardial progenitors and for Fgf8 signaling in the pharyngeal region.