Drosophila Melanogaster Lab Report

In this experiment, we observe and characterize the phenotype for white eyes (w-) in Drosophila melanogaster in order to determine the pattern of inheritance of the gene, which causes it. As well as this, we attempted to determine the mechanism for this mutation via literature review. The wild-type (w+) phenotype for eye color in D. melanogaster is red, with our mutants being white-eyed. Our initial hypothesis was that white eyes was an X recessive trait based on conclusions from experiments conduced by Thomas H. Morgan in 1909. Our experimental crosses over the course of this experiment indicated, however, that our trait is likely an X-linked recessive trait based on the phenotypes that we observed in each generation. Therefore, we conclude

This gene is part of a membrane-spanning system that is necessary for shuttling pigment molecules into pigment cells in the eyes. When this gene is activated, it shuts down two alternative pathways that would normally produce guanine-specific transporters and tryptophan specific transporters, which would have produced red to brown eye pigmentation. Depending on the exact mutation, this normally causes missense mutation(s) in helices important to these transporters. (Mackenzie et al. 1999). Regardless of the specific mutation, brown and red pigments, also known as ommochromes and pterins respectively, are greatly reduced in concentration which leads to white eyes, or eyes with a lack of pigmentation in the pigmentation cells. In organisms with wild-type eyes, or eyes with any pigmentation in them, these pathways are fully or partially functional and ommochromes and pterins can be transported into pigmentation cells normally. These ommochromes and pterins are the pigments that are responsible for color in the eye (Hanley et al. 1967). Therefore, my first hypothesis regarding the dysfunction of a single gene is more similar to the true mechanism than my second hypothesis suggesting a dual gene mediated pathway (Mackenzie et al.