Semester of Graduation

Fall 2023


Master of Biological Science (MBioSci)


Biological Sciences

Document Type



Several organs within the human body are tubular in structure. In the event of a malfunction in the development of these tubular structures, maladies like spina bifida, anencephaly, and several other defects can arise. To understand the mechanisms of tubular organ formation, we use the Drosophila embryonic salivary gland (SG) as a model. During embryogenesis, SG cells undergo a series of cell shape changes, like apical constriction, to accommodate the developing gland. Apical constriction is regulated in part by the signal of the secreted ligand Folded gastrulation (Fog) and its G protein-coupled receptor (GPCR) at the cell membrane, which leads to the activation of a RhoGEF, and then Rok in the medioapical region of the SG cell through RhoA (Rho1 in Drosophila) signaling. The RhoGEF(s) that mediate the GPCR and Rho signaling during apical constriction in the SG morphogenesis are unknown. We focus on four RhoGEFs, including RhoGEF2, Cyst, Puratrophin-1-like (Pura), and CG43658 due to their involvement in myosin activation during early embryogenesis (RhoGEF2 and Cyst) and their upregulated expression pattern in tubular organs (Pura and CG43658). Using a genetic suppression assay, we find that multiple RhoGEFs act downstream of Fog. Additionally, we are working on the characterization of Pura, as it potentially activates both Rho1 and Rac1 GTPases. Our preliminary data suggest that the longest isoform of Pura, Pura-PA, localizes in the apical domain of the SG cell, while its other isoforms localize cytoplasmically. Using transgenic lines containing the Pura-PA-specific N-terminal fragment, we find that the N-terminus is critical for recruitment to the apical domain. Together, these studies will help us continue to understand the complex mechanisms of Rho signaling regulation during tubular organ formation.



Committee Chair

SeYeon Chung

Available for download on Friday, November 01, 2024