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Toxoplasma gondii AP2IX-4 regulates gene expression during bradyzoite development

Sherri Huang, Michael J. Holmes, Joshua B. Radke, Dong-Pyo Hong, Ting-Kai Liu, Michael W. White, View ORCID ProfileWilliam J. Sullivan Jr.
doi: https://doi.org/10.1101/104208
Sherri Huang
1Department of Pharmacology & Toxicology
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Michael J. Holmes
1Department of Pharmacology & Toxicology
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Joshua B. Radke
3Departments of Molecular Medicine & Global Health, University of South Florida, Tampa, FL, USA
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Dong-Pyo Hong
3Departments of Molecular Medicine & Global Health, University of South Florida, Tampa, FL, USA
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Ting-Kai Liu
1Department of Pharmacology & Toxicology
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Michael W. White
3Departments of Molecular Medicine & Global Health, University of South Florida, Tampa, FL, USA
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William J. Sullivan Jr.
1Department of Pharmacology & Toxicology
2Microbiology & Immunology, Indiana University School of Medicine, Indianapolis, IN, USA
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  • ORCID record for William J. Sullivan Jr.
  • For correspondence: wjsulliv@iu.edu
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ABSTRACT

Toxoplasma gondii is a protozoan parasite of great importance to human and animal health. In the host, this obligate intracellular parasite persists as a tissue cyst form that is invisible to the immune response and unaffected by current therapies. The tissue cysts facilitate transmission through predation and give rise to chronic cycles of toxoplasmosis in immune compromised patients. Transcriptional changes accompany conversion of the rapidly replicating tachyzoites into the encysted bradyzoites, yet the mechanisms underlying these alterations in gene expression are not well-defined. Here we show that AP2IX-4 is a nuclear protein exclusively expressed in tachyzoites and bradyzoites undergoing division. Knockout of AP2IX-4 had no discernible effect on tachyzoite replication, but resulted in a reduced frequency of tissue cyst formation following alkaline stress induction – a defect that is reversible by complementation. AP2IX-4 has a complex role in regulating bradyzoite gene expression, as many bradyzoite mRNAs dramatically increased beyond normal stress-induction in AP2IX-4 knockout parasites exposed to alkaline media. The loss of AP2IX-4 also resulted in a modest virulence defect and reduced cyst burden in chronically infected mice, which was also reversed by complementation. These findings illustrate that the transcriptional mechanisms responsible for tissue cyst development operate across the intermediate life cycle from the dividing tachyzoite to the dormant bradyzoite.

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Posted January 30, 2017.
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Toxoplasma gondii AP2IX-4 regulates gene expression during bradyzoite development
Sherri Huang, Michael J. Holmes, Joshua B. Radke, Dong-Pyo Hong, Ting-Kai Liu, Michael W. White, William J. Sullivan Jr.
bioRxiv 104208; doi: https://doi.org/10.1101/104208
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Toxoplasma gondii AP2IX-4 regulates gene expression during bradyzoite development
Sherri Huang, Michael J. Holmes, Joshua B. Radke, Dong-Pyo Hong, Ting-Kai Liu, Michael W. White, William J. Sullivan Jr.
bioRxiv 104208; doi: https://doi.org/10.1101/104208

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