Discussion:

* The left-right axis patterning is very hard to detect in the embryos. Perhaps by staining regions of the embryo we would have been able to see the direction of the heart loop and such.

* We treated our embryos too early to see problems with truncation. Had we treated an additional set a later developmental stage we may have been able to see truncation in the embryos as a result of the cyclopamine.

*Cyclopamine clearly affected the development of the eyes. From this we conclude that sonic hedgehog is in fact a key player in the development of the eye in Medaka fish. This is in agreement with the model that has been developed for the role of SHH in eye formation in other vertebrates (Chiang et al., 1996). The model suggests that there is an optical field anywhere on which the eye cups can form. SHH is thought to be involved with the separation of this field into two distinct optical regions. By blocking the SHH signal one blocks this separation of the optical field. Depending on the degree to which the signal is block determines the degree to which the eyes are separated. This is why in some cases we saw full cyclopia and others only had fused eyes. This model however, does not account for the detached lenses seen in many of the embryos.

*Because there was no statistical significance between the control and treated embryos with circulatory defects we could not conclude that the cyclopamine was the agent affecting its formation. There were a lot of the control embryos with the same defect. For this reason we concluded that the circulatory defects were most likely do to the ethanol and not the cyclopamine. If we had more time to further