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		Introduction Lithium chloride is a known teratogen which alters development in a variety of organisms including sea urchins, Xenopus (frogs), and Brachydanio rerio (Zebrafish) (Gilbert, 2003). In sea urchin embryos, lithium chloride causes the accumulation of nuclear Beta-catenin in every cell, and transforms presumptive ectoderm into endoderm (Gilbert, 2003). Lithium exposure in cleavage-stage embryos of Xenopus inhibits dorsal/ventral axis specification and results in radially-symmetric, dorsal-anteriorized embryos (Stachel et. al., 2003). The research conducted by Stachel and colleagues suggests that lithium induction of pre-midblastular Zebrafish prevents normal dorsal/ventral axis patterning by acting as an inhibitor to the phosphoinositol pathway, which results in goosecoid and noggin expression outside the region of the presumptive embryonic shield instead of these genes being confined to the region proximal to the dorsal blastopore lip. Experiments by Stachel and colleagues have shown that the development of anterior structures is dependent on Wnt signaling, especially the transcription of goosecoid, which codes for a dorsalizing protein necessary for normal anterior development (Stachel et. al., 2003). The increase in gene expression of organizer-specific proteins such as Goosecoid in the presumptive ventral regions of the organism produces different phenotypic results when the induction occurs at certain stages in development (Stachel et. al., 1993). For instance, the exposure of embryos to LiCl before the midblastular transition (2 hour stage) results in hyperdorsalization and the inhibition of normal dorsal/ventral axis patterning (Deitrich, 1999). In contrast, embryos exposed to LiCl at the four-hour stage after the midblastular transition experienced normal dorsal/ventral axis specification but perturbed development of anterior structures such as eyes (Stachel et. al., 1993). The purpose of this experiment is to study the effects of lithium teratogenesis on post-midblastular embryo to observe whether or not the inhibition of anterior development occurs along a gradient, with increasing concentrations of lithium chloride leading to incrementally more severe defects in anterior development. Alternatively, there may be a certain threshold at which lithium induces defects in anterior development. Indications of the former hypothesis would consist of lithium teratogenesis leading to, for example, partial formation of an eye at one concentration and the complete absence of eye formation at a slightly higher concentration, then it may be possible that lithium teratogenesis affects development along a gradient. In accordance with the latter situation, the observable effects of lithium teratogenesis would consist in the complete absence of the eyes at one concentration and complete formation and presence of all eye structures including retina and lens at a slightly lower concentration. J. N. White 5/13/04