The chick embryo is a useful experimental system because it can be easily manipulated during early development. Imagine that you injected sonic hedgehog (Shh) into the optic vesicle of a chick embryo just prior to the onset of differentiation in the neural retina, and then you allowed the embryo to develop. How might the mature chick differ from a normal, untreated chick? Why?
(This is revised from the original post.)
The homeotic selector gene Antennapedia is known to specify the second thoracic segment of Drosophila melanogaster. This segment harbors a pair of legs and has no antenna or wings. In my lecture on Monday, I showed a picture of a mutant fly in which a pair of legs are sticking out form a head segment. In this form of mutant, the Antennapedia gene was expressed in the head, as well as in the thorax. So the mutant phenotype is considered as a gain-of-function phenotype, where ectopic expression of the gene in the head has caused a dominant phenotype. If the function of the Antennapedia gene is to promote the formation of the legs and to suppress the formation of antenna, what would happen in a different Antennapedia mutant where its normal expression in the thorax is lost (you could call this a recessive mutation)? Explain your answer.
-from Dr. Nakagawa
The next question is pretty straightforward. It might require that you review a little neuroanatomy.
Describe the embryological origin of the superior colliculus.
Imagine that you stably transfected a small group of cells at the margin of the posterior neural plate as indicated in the figure. You transfected the cells with a constitutively expressed reporter gene such as green fluorescent protein (GFP). All cells generated by the division of the transfected cells would express GFP. Thus, you can follow the lineage of the cells that you originally transfected. What cell type(s) in the adult would you expect to express GFP and where would you expect to find them?
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