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<dc:title xml:lang="fr">Étude de l’infection de la microsporidie Tubulinosema ratisbonensis sur son hôte Drosophila melanogaster : importance du métabolisme lipidique de l’hôte dans la prolifération parasitaire</dc:title>
<dcterms:alternative xml:lang="en">Study of Drosophila melanogaster infection by the microsporidia Tubulinosema ratisbonensis : importance of host lipid metabolism for the parasitic proliferation</dcterms:alternative>
<dc:subject xml:lang="fr">Drosophila melanogaster</dc:subject>
<dc:subject xml:lang="fr">Microsporidie</dc:subject>
<dc:subject xml:lang="fr">Métabolisme lipidique</dc:subject>
<dc:subject xml:lang="en">Drosophila melanogaster</dc:subject>
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<dc:subject xml:lang="en">Lipid metabolism</dc:subject>
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<dcterms:abstract xml:lang="fr">Nous étudions les interactions hôte/pathogène entre la drosophile et un parasite intracellulaire, la microsporidie Tubulinosema ratisbonensis.Les microsporidies dérivent du groupe des champignons possédant un génome réduit et pas de mitochondrie. Ces parasites dépendent fortement du métabolisme de leur hôte pour proliférer. Les interactions entre les microsporidies et leurs hôtes reste peu étudiées au niveau métabolique.In vivo, les spores ciblent beaucoup de tissues, en particulier le corps gras qui perd ces gouttelettes lipidiques. Les réserves métaboliques sont épuisées au cours de l’infection et les mouches présentent les caractéristiques de famine. La supplémentation en acide gras dans la nourriture des mouches infectées augmente la prolifération du parasite. Cet effet est bloqué lorsque l’on perturbe l’assimilation ainsi que le transport des lipides provenant de l’intestin. En conséquence, les mouches résistent mieux à l’infection lorsque la synthèse des lipides est bloquée.</dcterms:abstract>
<dcterms:abstract xml:lang="en">We study the host/pathogen interactions between Drosophila and a natural intracellular parasite : the microsporidium Tubulinosema ratisbonensis. Microsporidia are highly derived group of fungi with a compact genome and no mitochondria. These obligate parasites thus rely intensively on host metabolism for growth and proliferation. The interactions between microsporidia and their hosts remain poorly understood at the metabolic level.In vivo, spores target many tissues especially the fat body that loses its lipid droplets. Metabolic reserves become depleted during the course of the infection and flies display the hallmarks of severe starvation. Fatty acids supplementation of the infected flies diet increases parasite proliferation and host susceptibility to the parasite. This effect is blocked when perturbing lipid assimilation and transport originating from the gut. Accordingly, flies resist better infection when lipid synthesis is blocked, as the parasite proliferation is hampered.</dcterms:abstract>
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