CARDIAC MALFORMATION IN NEONATAL MICE LACKING CONNEXIN43

Gap junctions are made up of connexin proteins, which comprise a multi gene family in mammals. Targeted mutagenesis of connexin43 (Cx43), one of the most prevalent connexin proteins, showed that its absence was compatible with survival of mouse embryos to term, even though mutant cell lines showed reduced dye coupling in vitro. However, mutant embry os died at birth, as a result of a failure in pulmonary gas exchange c aused by a swelling and blockage of the right ventricular outflow trac t from the heart. This finding suggests that Cx43 plays an essential r ole in heart development but that there is functional compensation amo ng connexins in other parts of the developing fetus.