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First published online July 10, 2009
doi: 10.1242/10.1242/dev.038562

Development 136, 2665-2674 (2009)
Published by The Company of Biologists 2009
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Cx30.2 enhancer analysis identifies Gata4 as a novel regulator of atrioventricular delay

Nikhil V. Munshi1,2, John McAnally1, Svetlana Bezprozvannaya1, Jeff M. Berry1,2, James A. Richardson3, Joseph A. Hill1,2 and Eric N. Olson1,*

1 Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA.
2 Deparment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-9047, USA.
3 Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9072, USA.

* Author for correspondence (e-mail: Eric.Olson{at}UTSouthwestern.edu)

Accepted 1 June 2009

The cardiac conduction system comprises a specialized tract of electrically coupled cardiomyocytes responsible for impulse propagation through the heart. Abnormalities in cardiac conduction are responsible for numerous forms of cardiac arrhythmias, but relatively little is known about the gene regulatory mechanisms that control the formation of the conduction system. We demonstrate that a distal enhancer for the connexin 30.2 (Cx30.2, also known as Gjd3) gene, which encodes a gap junction protein required for normal atrioventricular (AV) delay in mice, is necessary and sufficient to direct expression to the developing AV conduction system (AVCS). Moreover, we show that this enhancer requires Tbx5 and Gata4 for proper expression in the conduction system, and Gata4+/- mice have short PR intervals indicative of accelerated AV conduction. Thus, our results implicate Gata4 in conduction system function and provide a clearer understanding of the transcriptional pathways that impact normal AV delay.

Key words: Cardiac conduction system, Arrhythmia, Atrioventricular Node, Cx30.2, Gata4, Mouse


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