• Login
    View Item 
    •   Athenaeum Home
    • University of Georgia Theses and Dissertations
    • University of Georgia Theses and Dissertations
    • View Item
    •   Athenaeum Home
    • University of Georgia Theses and Dissertations
    • University of Georgia Theses and Dissertations
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    The role of Ca2+ influx during Toxoplasma gondii egress from host cells

    Thumbnail
    Date
    2016-05
    Author
    Moore, Christina Ann
    Metadata
    Show full item record
    Abstract
    Toxoplasma gondii is an obligate intracellular parasite that can infect any nucleated cell. The parasite invades host cells, replicates inside a parasitophorous vacuole and egresses to invade more host cells. This lytic cycle is associated with the tissue damage that accompanies the acute infection and is linked to the pathology of toxoplasmosis. Fluctuations of cytoplasmic Ca2+ are linked to the activation of the cellular processes involved in each step of the lytic cycle. However, the mechanism by which cytoplasmic Ca2+ is stimulated preceding egress is unknown. Using genetic Ca2+ indicators expressed in the cytosol of the parasites and also in the host cell, we show that cytoplasmic Ca2+ increases in the intracellular parasites prior to both artificially stimulated and natural egress. We demonstrated that extracellular Ca2+ entry enhances the events surrounding egress and that specific Ca2+ peaks observed prior to egress could correspond to signaling pathways regulating this step.
    URI
    http://purl.galileo.usg.edu/uga_etd/moore_christina_a_201605_ms
    http://hdl.handle.net/10724/36273
    Collections
    • University of Georgia Theses and Dissertations

    About Athenaeum | Contact Us | Send Feedback
     

     

    Browse

    All of AthenaeumCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects

    My Account

    LoginRegister

    About Athenaeum | Contact Us | Send Feedback