ZFIN ID: ZDB-PUB-090424-26
Increased Hox activity mimics the teratogenic effects of excess retinoic acid signaling
Waxman, J.S., and Yelon, D.
Date: 2009
Source: Developmental dynamics : an official publication of the American Association of Anatomists   238(5): 1207-1213 (Journal)
Registered Authors: Waxman, Joshua, Yelon, Deborah
Keywords: zebrafish, retinoic acid, teratogen, hox, heart
MeSH Terms:
  • Animals
  • Embryo, Nonmammalian/abnormalities*
  • Embryo, Nonmammalian/drug effects
  • Embryo, Nonmammalian/metabolism
  • Embryonic Development/drug effects
  • Embryonic Development/genetics
  • Embryonic Development/physiology
  • Heart Defects, Congenital/genetics
  • Heart Defects, Congenital/metabolism*
  • Homeodomain Proteins/biosynthesis*
  • Homeodomain Proteins/genetics
  • Signal Transduction/genetics
  • Signal Transduction/physiology
  • Teratogens/toxicity
  • Tretinoin/toxicity
  • Zebrafish/abnormalities*
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Zebrafish Proteins/metabolism*
PubMed: 19384962 Full text @ Dev. Dyn.
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.