My research focuses on elucidating the genetic mechanisms underlying the formation and development of the corneal lens in Drosophila. More specifically, I am studying genes potentially responsible for a variant in which the normally curved lens becomes flat. Through this work, the Treisman Lab aims to gain a deeper understanding of the Drosophila visual system and its relevance to visual dystrophies in humans, whose visual systems share significant similarities.
The Treisman Lab at NYU Langone studies the visual system of the Drosophila (fruit fly) in order to learn more about the human visual system, as they share many similarities. One of the lab’s projects is focused on a mutation of the corneal lens that disrupts the fly’s vision. The Drosophila corneal lens is composed of several materials, including chitin, a sugar molecule, and is precisely organized into equal layers that allow for constructive interference of light, a mechanism necessary for photoreceptors to accurately process light. In 2022, the lab discovered that a knockdown of the transcription factor Blimp-1 led to a mutation in the Drosophila optic units, in which the normally curved lens became flat. After investigating the effects of the Blimp-1 knockdown, the Treisman Lab decided to focus on genes that encode for chitin, more specifically, a group of genes called Vajk1-4 that encode chitin-binding proteins. My job was to test the hypothesis that a Vajk1-4 deletion would cause the flat-lens mutation. A CRISPR/Cas9 system, followed by DNA extraction, Polymerase Chain Reaction, and Agarose Gel Electrophoresis, was used to identify a mutation in the Vajk1-4 genes. After creating a Vajk4 mutant and realizing it did not display any phenotypic changes, we can conclude that a deletion of Vajk4 on its own does not cause the flat-lens mutation. In the future, we will test a full Vajk1-4 deletion to see if a larger deletion is necessary to induce the flat-lens mutation.
