|ZFIN ID: ZDB-PUB-070806-9|
Molecular changes associated with teratogen-induced cyclopia
Loucks, E.J., Schwend, T., and Ahlgren, S.C.
|Source:||Birth defects research. Part A, Clinical and molecular teratology 79(9): 642-651 (Journal)|
|Registered Authors:||Ahlgren, Sara, Loucks, Evyn|
|Keywords:||zebrafish, cyclopia, gli, six3b, dlx3b, telencephalon|
|PubMed:||17647295 Full text @ Birth Defects Res. Part A Clin. Mol. Teratol.|
Loucks, E.J., Schwend, T., and Ahlgren, S.C. (2007) Molecular changes associated with teratogen-induced cyclopia. Birth defects research. Part A, Clinical and molecular teratology. 79(9):642-651.
ABSTRACTBACKGROUND: Exposure of zebrafish embryos to a number of teratogens results in cyclopia, but little is known about the underlying molecular changes. METHODS: Using zebrafish embryos, we compare the effects cyclopamine, forskolin, and ethanol delivered starting just before gastrulation, on gene expression in early axial tissues and forebrain development. RESULTS: Although all three teratogens suppress gli1 expression, they do so with variable kinetics, suggesting that while suppression of Shh signaling is a common outcome of these three teratogens, it is not a common cause of the cyclopia. Instead, all teratogens studied produce a series of changes in the expression of gsc and six3b present in early axial development, as well as a later suppression of neural crest cell marker dlx3b. Ethanol and forskolin, but not cyclopamine, exposure reduced anterior markers, which most likely contributes to the cyclopic phenotype. CONCLUSIONS: These data suggest that each teratogen exposure leads to a unique set of molecular changes that underlie the single phenotype of cyclopia.