Deciphering the role of Shh signaling in axial defects produced by ethanol exposure.

Background: The phenotype of embryos exposed to ethanol is complex and likely due to multiple alterations in developmental pathways. We have previously demonstrated that Sonic hedgehog signaling (Shh-s) was reduced in both chicken and zebrafish embryos when exposed to ethanol.

Methods: There are many tissues affected by embryonic ethanol exposure, and in this article we explore the development of axial tissues, using zebrafish embryos.

Molecular changes associated with teratogen-induced cyclopia.

Background: 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.