Canonical Wg/Wnt pathway regulates Wolbachia intracellular density in Drosophila
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Wolbachia are widely spread, maternally transmitted insect endosymbiotic intracellular bacteria. They have been implicated in the control of several insect transmitted diseases, including dengue, yellow fever, Zika and malaria. Effective pathogen suppression in the insect host is shown to be proportional to the intracellular levels of bacteria. Therefore, understanding the molecular mechanisms underlying Wolbachia accumulation within organisms is extremely important for future epidemic control and research. Using Drosophila as a model insect, our lab has previously observed Wolbachia tropism to stem cell niches. Current work has identified polar cells as an additional site of Wolbachia tropism and demonstrated that Wg/Wnt signaling is important for Wolbachia intracellular accumulation in these somatic cells. In this thesis, we first observed that the Wg/Wnt pathway protein Armadillo also controls Wolbachia levels in the germline cells, indicating the possibility of having a conserved molecular mechanism controlling Wolbachia. Using RNAi and small molecule inhibitors of Shaggy, another component of the canonical Wg/Wnt pathway, we demonstrate that the canonical Wg/Wnt signaling is essential for Wolbachia intracellular accumulation. Our investigation provides fundamental insights into the mechanisms of Wolbachia intracellular accumulation. Furthermore, it offers novel strategies to modulate Wolbachia in non-model insect species, including various disease transmitting Anopheles, Culex, and Aedes. These findings potentially will increase the effectiveness of a Wolbachia-based vector transmitted disease suppression.