Transcriptional Regulation in the Mouse Atrioventricular Conduction System

  1. Derek J. Chadwick Organizer and
  2. Jamie Goode
  1. Angela V. Edwards1,
  2. Dorene L. Davis1,
  3. Amy L. Juraszek2,
  4. Andy Wessels2 and
  5. John B. E. Burch1

Published Online: 7 OCT 2008

DOI: 10.1002/0470868066.ch11

Development of the Cardiac Conduction System: Novartis Foundation Symposium 250

Development of the Cardiac Conduction System: Novartis Foundation Symposium 250

How to Cite

Edwards, A. V., Davis, D. L., Juraszek, A. L., Wessels, A. and Burch, J. B. E. (2003) Transcriptional Regulation in the Mouse Atrioventricular Conduction System, in Development of the Cardiac Conduction System: Novartis Foundation Symposium 250 (eds D. J. Chadwick and J. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/0470868066.ch11

Author Information

  1. 1

    Department of Cell and Developmental Biology, Fox Chase Cancer Center, Philadelphia, Pennsylvania, PA 19111, USA

  2. 2

    Department of Cell Biology and Anatomy, Cardiovascular Developmental Biology Center, Medical University of South Carolina, Charleston, SC 29425, USA

Publication History

  1. Published Online: 7 OCT 2008
  2. Published Print: 20 JUN 2003

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780470850350

Online ISBN: 9780470868065

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Summary

We identified a GATA6 gene enhancer that selectively marks the developing atrioventricular conduction system (AVCS) in transgenic mice. This enhancer reads anterior/posterior and medial/lateral positional information early in the cardiogenic programme and remains active in progressively more restricted subsets of heart cells leading up to AVCS formation. Additional experiments will be required to determine if the potential to be recruited into the AVCS is similarly restricted to a subset of myocardial cells early in the cardiogenic programme or if this enhancer can also be activated de novo in cells that initially reside outside this field. We are using several strategies to identify factors that regulate this and other AVCS enhancers and hence govern AVCS function. We are also using this enhancer to make transgenic mice that express Cre, or an inducible form of Cre, to track lineages and to delete floxed genes in the developing or mature AVCS. This Cre/lox approach provides a means to deconstruct complex congenital heart phenotypes that involve the conduction system and to test whether genes are required to form the AVCS or to maintain AVCS function. Lastly, we are exploring strategies to isolate and analyse AVCS cells from normal and affected hearts.