Increased Hox activity mimics the teratogenic effects of excess retinoic acid signaling

Authors

  • Joshua S. Waxman,

    1. Developmental Genetics Program and Department of Cell Biology, Kimmel Center for Biology and Medicine at the Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York
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  • Deborah Yelon

    Corresponding author
    1. Developmental Genetics Program and Department of Cell Biology, Kimmel Center for Biology and Medicine at the Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York
    • Developmental Genetics Program and Department of Cell Biology, Kimmel Center for Biology and Medicine at the Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016
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Abstract

Excess retinoic acid (RA) signaling can be teratogenic and result in cardiac birth defects, but the cellular and molecular origins of these defects are not well understood. Excessive RA signaling can completely eliminate heart formation in the zebrafish embryo. However, atrial and ventricular cells are differentially sensitive to more modest increases in RA signaling. Increased Hox activity, downstream of RA signaling, causes phenotypes similar to those resulting from excess RA. These results suggest that Hox activity mediates the differential effects of ectopic RA on atrial and ventricular cardiomyocytes and may underlie the teratogenic effects of RA on the heart. Developmental Dynamics 238:1207–1213, 2009. © 2009 Wiley-Liss, Inc.

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