Student Speaker

Lamp1 Deficiency Disrupts Lipid Transport in Drosophila

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Abstract

Lysosomes play an important role in cell homeostasis through the degradation and recycling of macromolecules. Many neurodegenerative diseases have been linked to defective lysosomes. Lysosome-associated membrane proteins, LAMP1 and LAMP2 in humans, have been well characterized for their role in autophagy and cholesterol transport in vertebrates, which play a role in the organism’s viability. Recently, analysis of the LAMP ortholog in Drosophila melanogaster, Lamp1, showed that Lamp1 mutant third instar larvae accumulate diacylglycerols with mid-chain fatty acids (mcDAGs) and sterols. mcDAGs are used exclusively in inter-organ lipid transport through the hemolymph in Drosophila. Thus, we hypothesize that the Lamp1 deficiency causes defects in lipid transport. To further study the effect of Lamp1 defects on lipid metabolism, we used light, fluorescence, and electron microscopy to visualize neutral lipids within the enterocytes of the 3rd instar larvae midgut. Mutant enterocytes displayed an increase in lipid accumulation, and this increase resulted in fewer yet larger lipid droplets in the anterior portion of the mutant midgut. Additionally, a shortening of microvilli length was observed in the mutant strain. An acidic lipase assay on larvae gut tissue showed increased lipase in the Lamp1 midgut. Our results suggest that Lamp1 plays a role in lipid transport, and the effects seen within the enterocytes of the mutant suggest that lipids are not able to be exported from enterocytes to other tissues when Lamp1 is missing