The cardiac conduction system (a tract of cardiomyocytes that propagates electrical impulses through the heart) coordinates heart contractions. Abnormalities in this system cause life-threatening arrhythmias but the molecular basis of its development is poorly understood. Now, Eric Olson and colleagues report that the transcription factor Gata4 regulates the system's development (see ). Atrioventricular (AV) delay (delayed impulse propagation through a structure called the AV node) coordinates atrial and ventricular contraction. In mice, AV delay requires expression of the gap junction protein connexin 30.2 (Cx30.2) in the AV conduction system. The authors identify an enhancer in the Cx30.2 gene that is necessary and sufficient to direct its expression to the developing AV conduction system, and show that its correct expression requires the Gata4 and Tbx5 transcription factors. Furthermore, Gata4+/- mice have faster AV conduction than their wild-type littermates. Overall, these results reveal an unexpected role for Gata4 in normal AV conduction and might bring the development of effective anti-arrhythmia drugs closer.
