Our laboratory combines studies in chick and mouse embryos with in vitro cell culture strategies to address the role of new genes in the development of the cardiovascular system and in particular the morphogenesis of the heart. Our recent work has examined the role of AT-rich interactive domaincontaining protein 3B (Arid3b) during heart formation. Arid3b is a transcription factor of the highly conserved ARID family, whose members share a common DNA-binding domain. Arid3b null-mice die early in embryonic development and their phenotype includes severe defects in many structures, especially the heart. However, the exact roles of Arid3b in development remain unclear.

Examination of the pattern of Arid3b expression shows that it is expressed at early stages of development in the heart tube and is later restricted to the myocardium of the outflow tract, right ventricle, atria and sinus venosus. We are currently carrying out anatomical, histological, cellular and molecular analyses to characterize the cardiac defects produced by the absence of the Arid3b gene. Our results so far identify a major defect in outflow tract formation in Arid3b knockout mice.

Our data also indicate that Arid3b regulates the contribution to the heart of cells from the secondary heart field. We plan to analyze the cellular basis of these Arid3b functions—for example its possible involvement in cell migration—and to identify its molecular targets by microarray analyses.