Increased Hox activity mimics the teratogenic effects of excess retinoic acid signaling
- Waxman, J.S., and Yelon, D.
- Developmental dynamics : an official publication of the American Association of Anatomists 238(5): 1207-1213 (Journal)
- Registered Authors
- Waxman, Joshua, Yelon, Deborah
- zebrafish, retinoic acid, teratogen, hox, heart
- MeSH Terms
- 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
- Zebrafish Proteins/metabolism*
- 19384962 Full text @ Dev. Dyn.
Waxman, J.S., and Yelon, D. (2009) Increased Hox activity mimics the teratogenic effects of excess retinoic acid signaling. Developmental dynamics : an official publication of the American Association of Anatomists. 238(5):1207-1213.
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
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes