Date of Award

12-16-2016

Degree Type

Thesis

Degree Name

Honors Thesis

Department

Biology

First Advisor

Lindsay Lewellyn

Abstract

Infertility is a widespread condition that does not always have a known cause, and for which we often do not have a cure. One potential cause of infertility is defects in gametogenesis, or the formation of sperm and egg. During gametogenesis in most organisms, the developing sperm and egg are connected to each other or to supporting cells through intercellular bridges, allowing transfer of materials between cells. Defects in these connections can lead to infertility. The developing fruit fly egg is an excellent model system to study intercellular bridges, or ring canals. Rich in f-actin and actinbinding proteins, ring canals expand ~20 fold during oogenesis, and this expansion is accompanied by a 134-fold increase in the amount of actin in the structure. Ring canal expansion depends on the Arp2/3 complex; mutations in Arp2/3 complex members lead to decreased expansion and ring canal collapse. Interestingly, the Arp2/3 mutant phenotype has been reported to affect later stages of oogenesis (beginning at stage 5). This suggests that other actin nucleators could be involved in promoting ring canal growth prior to this point. I have characterized a role for the formin-family actin nucleator, Diaphanous (Dia), during oogenesis. Depletion of Dia leads to defects in normal ring canal structure and expansion, which are distinct from those observed following depletion of the Arp2/3 complex members. Future work will determine the mechanisms that promote the localization and activation of Arp2/3 and Diaphanous in the context of ring canal formation and expansion.

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