Purine Sensing and Starvation Response in Toxoplasma gondii
Bennett, Charlotte
Bennett, Charlotte
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Abstract
Toxoplasma gondii is an obligate intracellular parasite estimated to infect one-third of people globally. Immunocompromised individuals and fetuses are at the highest risk of developing severe toxoplasmosis. Treatment remains difficult because the parasite's complex life cycle allows tachyzoites (acute stage) to differentiate into bradyzoites (chronic tissue cyst stage). Current therapies fail to eliminate or prevent cyst formation, leaving toxoplasmosis incurable. T. gondii depends entirely on its host cell for nutrients, including purines required for nucleic acid synthesis and metabolic function. Unlike mammalian cells, T. gondii cannot synthesize purines de novo, presenting a metabolic vulnerability that could be exploited therapeutically. However, the parasite�s mechanisms for sensing and regulating purine availability remain poorly understood. This project characterizes parasite replication in response to adenosine starvation and reintroduction using a newly adapted live-parasite fluorescence assay. The role of a T. gondii homolog of the mammalian nucleoside?sensing growth regulator TOR was also preliminarily examined by generating a knockdown strain. Results suggest that T. gondii can likely recover from prolonged adenosine starvation, though concentrations required to induce starvation or normal growth vary by host cell and parasite strain, among other factors. Additionally, increased parasite growth at 0.25 and 1�M adenosine compared to higher concentrations indicates a potential uptake of purines made available by starvation-induced host-cell autophagy. Though further work is needed to confirm TOR knockdown success and validate the observed adenosine starvation and recovery phenotypes, these results are an important advance in our understanding of the parasite�s response to purine starvation. Comparing signaling patterns in adenosine-starved vs. non-starved parasites may reveal important regulators of growth or differentiation into bradyzoites. Unravelling this signaling network may reveal key differences from mammalian cell growth regulation, exposing targets for potentially curative toxoplasmosis therapies.
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Date
1/1/2026
Student Status
Senior (Graduating in 2026)
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Poster
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Microbiology and Molecular Genetics
College/School
College of Agriculture and Life Sciences
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Life Science