PUBLICATION

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

Authors
Waxman, J.S., and Yelon, D.
ID
ZDB-PUB-090424-26
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.
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.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping