Increased Hox activity mimics the teratogenic effects of excess retinoic acid signaling
Article first published online: 21 APR 2009
Copyright © 2009 Wiley-Liss, Inc.
Volume 238, Issue 5, pages 1207–1213, May 2009
How to Cite
Waxman, J. S. and Yelon, D. (2009), Increased Hox activity mimics the teratogenic effects of excess retinoic acid signaling. Dev. Dyn., 238: 1207–1213. doi: 10.1002/dvdy.21951
- Issue published online: 21 APR 2009
- Article first published online: 21 APR 2009
- Manuscript Accepted: 9 MAR 2009
- NHLBI/NIH. Grant Numbers: R01 HL069594, F32 HL083591, K99 HL091126
- retinoic acid;
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.