Date of Award


Degree Type


Degree Name

Honors Thesis



First Advisor

Lindsay Lewellyn


Infertility is a prevalent issue in the United States, impacting 1.5 million women (1). A possible cause of infertility is defects in gametogenesis, or the formation of sperm and egg. Therefore, understanding the basic mechanisms that promote normal gamete formation could impact our understanding of infertility. The Drosophila melanogaster egg develops from an organ-like structure called an egg chamber. The egg chamber is composed of a central cluster of 16 germ cells that are connected to one another by intercellular bridges, called ring canals. These ring canals are composed of filamentous actin and allow the transfer of materials from supporting nurse cells to the developing oocyte. The ring canals form during early oogenesis and then expand 20-fold. Defects in ring canal formation or expansion can lead to infertility. The purpose of this project was to determine the role of the SH2/SH3 adaptor protein, Dreadlocks (Dock), in the germline ring canals of the developing Drosophila egg. Dock is involved in the formation of other actin-rich structures and has been shown to interact with other known ring canal proteins; thus, I examined whether depletion or mutation of Dock affected the process of nurse cell dumping or the size of the ring canals throughout development. Depletion of Dock by RNA interference (RNAi) caused an over-expansion of the outer diameter of the ring canals in egg chambers between the stages of 6 and 10b of oogenesis. Reducing Dock levels also enhanced the phenotype caused by depletion of two other ring canal components, the kinase Misshapen or the Arp2/3 complex. This led me to propose that Dock functions with Misshapen and the Arp2/3 complex to promote normal ring canal expansion and stability. Because of the conserved nature of these intercellular bridges and the proteins being studied, this work could provide significant insight into gametogenesis in higher organisms.