What effects would you expect to see on the sizes of various areas of the telencephalon-primary visual cortex, primary somatosensory cortex, and frontal/motor cortex-if Wnt signaling were inhibited during anteroposterior patterning of the neural tube?

If a mutation were to occur to disrupt the localization of ankyrinG, such that this protein became distributed throughout the Purkinje cell body and axon, what phenotype would you expect? Briefly explain your reasoning, assuming that the mutation does not disrupt interactions between ankyrinG and neurofascin.

What might you expect to observe if multiple neurons were experimentally manipulated to express exactly the same combination of Dscam exons? Briefly explain your reasoning.