Swapping Connexin Genes How Big Is the Gap?

Manipulation of the expression of specific genes intransgenic or knockout (KO) mice has become animportant strategy to study the biological and physiological roles of individual cardiac proteins.1–3 Several laboratories using transgenic and knockout methodologies have made substantial progress in generating mouse models with reduced connexin expression in the heart. This has provided the unique opportunity to characterize both qualita-tively and quantitatively the role of cardiac gap junction channels in electrical wave propagation and has opened many interesting questions regarding the electrophysiological con-sequences and proarrhythmic effects of reduced intercellular coupling in the atria, ventricles, and His-Purkinje system of neonatal and/or adult mice lacking a given connexin. The current count of 19 connexins in the mouse genome and 20 connexins in the human genome4 implies a highly intriguing diversity of connexin function. But the exact natur