Beck, EmilyCresko, WilliamNiebergall, Emily2019-06-172019-06-17https://hdl.handle.net/1794/24637Single page posterT-cell deficiencies cause cell-mediated immunodeficiencies including Severe Combined Immunodeficiency (SCID) and DiGeorge Syndrome. Understanding cell-mediated deficiency is complicated by the invasive nature of prenatal tests and by the large role genetic variation plays in etiologies of immune disease. Development of an outbred immunogenetics model system is therefore needed to understand how genetic variation impacts phenotypic variation of immune disease. Threespine stickleback fish (Gasterosteus aculeatus) provide just such a model, with divergent natural populations harboring high levels of genetic and phenotypic variation. Importantly, external fertilization and transparent development of large numbers of progeny facilitate the study of immune cell development in a less labor intensive manner to mammalian systems. However, the timing of onset of the adaptive immune system is currently unknown in stickleback. To identify onset of adaptive immunity, we will analyze gene expression of early activators of adaptive immunity in genetically divergent lines of stickleback. These include V(D)J recombination activating genes, rag1 and rag2, and T cell receptor progenitor genes, tcr-β and tcr-γ. To analyze when expression of these genes is initiated, we will perform rtPCR and in situ hybridization in a developmental time series. Knowing when adaptive immunity onset occurs advances threespine stickleback as an immunogenetics disease model, allowing manipulative studies of immunological phenotypes in the context of genetic variation.Creative Commons BY-NC-ND 4.0-USUndergraduate Research SymposiumImmunologyFish