Investigating the role of Sep2 in branching morphogenesis and seamless tubulogenesis

Abstract

Tubular networks are implicated in the function of multiple organs, arising from diverse tube topologies. Branching morphogenesis and tubulogenesis of these seamless tubes are processes that remain open to further investigation. The tracheal system of Drosophila melanogaster is an exemplary model of tubular networks that arise from seamless or unicellular tubes; its terminal cells have even been evidenced in cytoskeletal mechanisms of tube formation. Septins are GTP-binding proteins that function by associating with themselves and other cytoskeletal components, such as microtubules and actin. By facilitating crosstalk between actin and microtubules, which are heavily involved in cell elongation and lumen growth, septins like Sep2 become compelling effectors of seamless tube formation. Preliminary findings indicate that Sep2 is required for proper branching morphology and for the coupling of branch and lumen growth in Drosophila terminal cells. In the following research, we characterize the phenotype of Sep2 knockdown using two distinct RNAi lines and confirm RNAi silencing of Sep2. A Sep109 mutant allele is identified in CRISPR-edited fly lines and its effects are characterized in tracheal terminal cells. Further experimentation with septin depletion helps elaborate on the role of these proteins in the mechanisms that underlie the formation of seamless tubes.