Open Access Dissertation
Date of Award
Lori A. Pile
Sin3A has been previously shown to be an essential gene for Drosophila viability and is implicated in the regulation of cell cycle. In this study, we show that SIN3 is not only required for embryonic viability but also for post-embryonic development. Genetic analysis suggests that the different isoforms of SIN3 may regulate unique sets of genes during development. The developmental lethality occurring due to ubiquitous knock down of SIN3 is hypothesized to be to the result of defects in cell proliferation. Conditional knock down of SIN3 in the wing discs results in a curly wing phenotype in the adult fly. These wings are smaller and have fewer cells resulting from a defect in cell proliferation. This is visualized in the form of smaller SIN3 knockdown clones in the wing discs. Furthermore, loss of SIN3 results in a decrease in the number of mitotic cells in the wing discs. This is in part due to misregulation of the G2/M phase of the cell cycle. SIN3 genetically interacts with STG, a protein important for the G2/M phase of the cell cycle. Loss of SIN3 results in downregulation of STG whereas overexpression of STG in a SIN3 knockdown background is able to rescue the curly wing phenotype. SIN3 also genetically interacts with other genes involved in the cell cycle like Cdk2 and Cdc16 suggesting that SIN3 plays a role in multiple phases of the cell cycle. SIN3 also genetically interacts with genes involved in the Wnt and Toll signaling pathways, the mediator accessory sub complex, transcription regulation and chitin metabolism. These results suggest that SIN3 not only plays a role in regulating the cell cycle but also other processes during development.
Swaminathan, Aishwarya, "Analysing The Effects Of Loss Of Sin3 In Drosophila Melanogaster" (2010). Wayne State University Dissertations. 125.