Adaptation to low parasite abundance affects immune investment and immunopathological responses of cavefish
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ABSTRACT:
PROVIDER: PRJNA527091 | ENA |
REPOSITORIES: ENA
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Project description:Reduced parasitic infection rates in the developed world are suspected to underlie the rising prevalence of autoimmune disorders. However, the long-term evolutionary consequences of decreased parasite exposure on an immune system are not well understood. We used the Mexican tetra Astyanax mexicanus to understand how loss of parasite diversity influences the evolutionary trajectory of the vertebrate immune system, by comparing river with cave morphotypes. Here, we present field data affirming a strong reduction in parasite diversity in the cave ecosystem, and show that cavefish immune cells display a more sensitive pro-inflammatory response towards bacterial endotoxins. Surprisingly, other innate cellular immune responses, such as phagocytosis, are drastically decreased in cavefish. Using two independent single-cell approaches, we identified a shift in the overall immune cell composition in cavefish as the underlying cellular mechanism, indicating strong differences in the immune investment strategy. While surface fish invest evenly into the innate and adaptive immune systems, cavefish shifted immune investment to the adaptive immune system, and here, mainly towards specific T-cell populations that promote homeostasis. Additionally, inflammatory responses and immunopathological phenotypes in visceral adipose tissue are drastically reduced in cavefish. Our data indicate that long-term adaptation to low parasite diversity coincides with a more sensitive immune system in cavefish, which is accompanied by a reduction in the immune cells that play a role in mediating the pro-inflammatory response.
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Project description:Cell lines have become an integral resource and tool for conducting biological experiments ever since the Hela cell line was first developed (1). They not only allow detailed investigation of molecular pathways but are faster and more cost-effective than most in vivo approaches. The last decade saw many emerging model systems strengthening basic science research. However, lack of genetic and molecular tools in these newer systems pose many obstacles. Astyanax mexicanus is proving to be an interesting new model system for understanding metabolic adaptation. To further enhance the utility of this system, we developed liver-derived cell lines from both surface-dwelling and cave-dwelling morphotypes. In this study, we provide detailed methodology of the derivation process along with a comprehensive biochemical and molecular characterization of the cell lines, which reflects key metabolic traits of cavefish adaptation. We anticipate these cell lines to become a useful resource for the Astyanax community as well as researchers investigating fish biology, comparative physiology, and metabolism.
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Project description:we report a transcriptome-wide comparative investigation between surface and cave species in Sinocyclocheilus. De novo transcriptome assemblies were performed on surface and cave species; then the Sinocyclocheilus contigs were annotated with Gene Ontology. RNA-Seq assays revealed reduced transcription of a series of visual phototransduction and retinal disease related genes in cave-dwelling species compared with surface species. Degeneration of the retina in Sinocyclocheilus cavefish might occur in a lens-independent way by the down-regulation of several transcriptional factors, which have direct roles in retina development and maintenance, such as crx, rorb and Wnt pathway members. Examination of 2 different eye samples in 2 Sinocyclocheilus species.
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Project description:The ability to respond to stressful host environments is crucial for the survival of intracellular pathogens, during which transporters play key roles in the nutrient scavenging, such as lipid uptake. Here we discover a conserved malarial gene that orchestrates the parasitic adaption in the terminally differentiated, phospholipid scarce erythrocytes. The expression level of this gene, here named CAP, is the intensively upregulated in the erythrocyte-infecting parasites than the reticulocyte-infecting counterparts. We show that CAP encodes a small protein exported onto the membrane of infected erythrocytes where it interacts with host CTL1, a choline and ethanolamine transporter, and upregulates biosynthesis of phosphatidylcholine and phosphatidylethanolamine, the major component of parasite membrane. Deletion of CAP causes Plasmodium to upturn reticulocyte invasion and sexual stage differentiation. This work presents a novel mechanism for intracellular parasite to import lipid precursors into parasitized cells by manipulating an endogenous host transporter.
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