The role of Matrix metalloproteinase-2 in Drosophila melanogaster prepupal and pupal fat body autophagy
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Autophagy is the mechanism by which an organism can dispose of parts of its cells. This mechanism plays a vital role in many human diseases such as cancer and neurodegenerative diseases, includings Alzheimer's disease (Lőrincz et al., 2017). In order to examine how autophagy is regulated I studied it during metamorphosis in the model organism Drosophila melanogaster. Both D. melanogaster and humans have Matrix metalloproteinases, or MMPs, which are enzymes that work in the extracellular matrix (ECM) to cleave and degrade proteins. D. melanogaster has two distinct MMPs, MMP1 and MMP2. There is already evidence suggesting that MMP2 in D. melanogaster is involved in the ecdysone and insulin signalling pathways that lead to fat body remodeling (Bond et al., 2011). However, there has not been enough research done on whether MMP2 is involved in fat body autophagy. I propose an experiment to test whether MMP2 is required for fat body autophagy during the prepupal and pupal stages of metamorphosis. To do this I used the UAS-Gal4 system in conjunction with RNAi technology to generate flies that lack MMP2 in their fat body cells. I used a western blotting approach to quantify levels of autophagy in fat body cells from transgenic Drosophila that lack MMP2, and in the fat body cells from control, wild-type Drosophila (Lőrincz et al., 2017). My preliminary results suggest that MMP2 is required for fat body remodeling, but more research must be done to confirm this. Determining whether membrane type MMPs like MMP2 are involved in the signalling cascade leading to autophagy could be vital in determining how autophagy is triggered and in finding ways to treat the diseases associated with autophagy.