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C. Elegans Identified Upregulation of Lipid Metabolites in Three Lipid Biosynthesis Pathways: Phosphatidylcholines, Acylcarnitines and Ceramides

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C. Elegans Identified Upregulation of Lipid Metabolites in Three Lipid Biosynthesis Pathways: Phosphatidylcholines, Acylcarnitines and Ceramides Characterizing the role of host lipid metabolism on microsporidia infection in Caenorhabditis elegans by JiHae Jeon A thesis submitted in conformity with the requirements for the degree of Master's of Science Graduate Department of Molecular Genetics University of Toronto © Copyright by JiHae Jeon 2021 Characterizing the role of host lipid metabolism on microsporidia infection using the nematode Caenorhabditis elegans JiHae Jeon Master’s of Science Department of Molecular Genetics University of Toronto 2021 Abstract Microsporidia are fungal obligate intracellular pathogens that primarily manifest in immunocompromised individuals. Microsporidia have reduced metabolic capabilities and so they have strong host-dependence for many metabolic processes. However, despite their growing medical importance, microsporidia are poorly understood. I investigated the impact of host lipid metabolism on microsporidia infection using the nematode Caenorhabditis elegans and its natural microsporidian pathogen Nematocida parisii. A previous metabolomics screen performed on N. parisii infected C. elegans identified upregulation of lipid metabolites in three lipid biosynthesis pathways: phosphatidylcholines, acylcarnitines and ceramides. I also identified an increase in the level of lipid droplet associated lipase, ATGL-1, upon infection. In addition, by screening 25 lipid mutant strains, animals defective in producing sphingosine showed resistance to infection whereas supplementing sphingosine increased susceptibility, suggesting sphingosine may be involved in promoting microsporidian growth. Together, my research of lipid regulation by microsporidia can help to determine new therapeutic targets for microsporidian infection. ii Acknowledgment First and foremost, I’d like to thank my supervisor, Dr. Aaron Reinke, for giving me the opportunity to do this project in his lab and his continual support and guidance throughout my master’s degree. He has been an amazing mentor and his commitment and enthusiasm to science are truly inspirational. I am truly thankful for the opportunity to work in his lab. I would also like to thank Dr. Nick Burton for his work on lipid metabolomics and my committee members, Dr. Brent Derry, Dr. Greg Fairn, and Dr. Amy Caudy for their valuable insights and guidance on my project. I am thankful for their thoughtful questions that helped me shape my critical thinking skills. I would like to thank the entire Reinke lab for all the support and assistance they have offered me through the development of my work. Their helpful guidance and input helped me to survive the day-to-day life of grad school. I am grateful for all the meaningful conversations and good times (the usual all-you-can-eat sushi) I have shared with all of them. Thank you to all of my incredible friends, Nuri who cheered me up all the way from Waterloo, and especially my boyfriend, Simon, who always provided me with emotional support and encouragement. Thank you for being one of my biggest supporters. Last but not the least, I would like to thank my parents, my sister and my grandmother, without whom, none of this would’ve been possible. Thank you to my sister, Alice, who always surprised me with treats whenever I am down. Finally, to my parents and grandmother especially, I thank you most ardently for your continuous support of my aspirations. I am forever indebted to my parents for giving me the opportunities and experiences that have made me who I am. iii Table of Contents ACKNOWLEDGMENT ............................................................... III LIST OF TABLES ........................................................................ VII LIST OF FIGURES .................................................................... VIII LIST OF ABBREVIATIONS ........................................................ IX CHAPTER 1: INTRODUCTION .................................................... 1 1.1 Microsporidia .............................................................................................. 1 1.1.1 History .................................................................................................... 1 1.1.2 Microsporidia genome reduction ............................................................ 1 1.1.3 Developmental morphology and life cycle ............................................. 3 1.1.4 Microsporidia infections in humans ....................................................... 5 1.1.5 Microsporidia infections in C. elegans and N. parisii ............................ 5 1.2 Lipid Metabolism and host-pathogen interaction .................................... 7 1.2.1 Lipid metabolism in C. elegans .............................................................. 7 1.2.1.1 Phosphatidylcholine biosynthesis and function ................................................... 8 1.2.1.2 Sphingolipid biosynthesis and function ............................................................... 9 1.2.1.3 Carnitine shuttle and function ............................................................................ 10 1.2.2 Lipid metabolism in microsporidia ....................................................... 11 1.2.3 Importance of lipids in parasitic infection ............................................ 12 1.3 Thesis Rationale ......................................................................................... 14 CHAPTER 2 MATERIALS AND METHODS ............................ 16 2.1 Materials and Methods ............................................................................. 16 2.1.1 Nematode strains and microsporidia culture ........................................ 16 2.1.1.1 C. elegans strains ............................................................................................... 16 2.1.1.2 N. parisii spore preps ......................................................................................... 17 2.2 Fasting experiment ................................................................................... 18 2.3 Lipid staining ........................................................................................... 18 iv 2.3.1 Oil red O staining .................................................................................................. 18 2.4 Microsporidian infection experiment ....................................................... 19 2.4.1 Optimizing infection conditions ........................................................................... 19 2.4.2 24h, 48h, and 72h infection with atgl-1::gfp ....................................................... 19 2.4.3 Infection assay between atgl-1::gfp and atgl-1(P87S) ......................................... 20 2.4.4 Lipid mutants N. parisii infection ......................................................................... 20 2.4.5 Pulse-infection assay ............................................................................................ 20 2.4.6 DY96 and FISH staining using PFA fix ............................................................... 21 2.4.7 DY96 staining using acetone fix ........................................................................... 21 2.4.8 FISH staining using acetone fix ............................................................................ 21 2.5 Immunofluorescent Microscopy .............................................................. 22 2.5.1 Live imaging and Quantification .......................................................................... 22 2.5.2 Oil red O Quantification ....................................................................................... 22 2.5.3 Embryo count and pathogen load analysis by DY96 ............................................ 22 2.5.4 Pathogen load and sporoplasm analysis by FISH ................................................. 22 2.5.5 Brood count analysis and Synthetic effects score calculation .............................. 23 2.6 Sphingosine Supplementation .................................................................. 23 2.7 Lipid metabolite quantification ................................................................ 24 CHAPTER 3 RESULTS ................................................................. 24 3.1 Introduction ............................................................................................... 24 3.2 Understanding changes in host lipid metabolism in response to microsporidia infection ................................................................................... 27 3.2.1 ATGL-1 is upregulated in response to fasting ...................................... 27 3.2.2 The level of ATGL-1 increases in a time-dependent manner upon microsporidian infection ................................................................................ 29 3.2.3 Lipid stores are reduced in response to N. parisii infection, but the function of ATGL-1 is unknown. .................................................................. 31 3.3 Characterizing the impact of host lipid metabolism on microsporidia infection ............................................................................................................ 36 3.3.1 Various lipid metabolites are upregulated upon N. parisii infection .... 36 3.3.2 A screen of 25 lipid mutants identifies lipid metabolites involved in resistance or hypersusceptibility to microsporidian infection ....................... 39 3.3.3 Sphingosine supplementation increases susceptibility of C. elegans to N. parisii infection ......................................................................................... 46 3.3.4 Sphingolipid
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