This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. ***Please note Dr. Mariana Matrajt's funding was terminated as of 8/31/09.*** The human pathogen Toxoplasma gondii is one of the most widely distributed protozoan parasites, infecting approximately one-third of the world's population. Asexual replication of T. gondii in humans and intermediate hosts is characterized by two forms: rapidly growing 'tachyzoites'and latent 'bradyzoite'tissue cysts. Tachyzoites are responsible for acute illness and congenital neurological birth defects, while the more slowly dividing bradyzoite form can remain latent within the tissues for many years, representing a threat to immunocompromised patients. The interconversion between tachyzoites and bradyzoites, at the heart of parasite survival and pathogenicity, is poorly understood at a genetic and molecular level, which makes understanding this process an important goal. We are interested in identifying genes involved in the bradyzoite differentiation process in order to better understand the biology of the conversion between tachyzoites and bradyzoites. To this end we have successfully developed a genetic screen to identify regulatory genes that control parasite differentiation and have isolated mutants that fail to convert to bradyzoites under differentiation conditions. Seven of these mutants were selected for further characterization and microarray analysis. All these mutants show significantly increased replication rates and reduced expression of bradyzoite markers which are features that confirm that indeed these mutants have defects forming bradyzoites. In the previous report we described the microarray analysis carried out with these seven mutants. In the past year we finished the analysis of the microarray data and recently submitted this work for publication. The summary of this work is as follows:

National Institute of Health (NIH)
National Center for Research Resources (NCRR)
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Special Emphasis Panel (ZRR1-RI-B (01))
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University of Vermont & St Agric College
Internal Medicine/Medicine
Schools of Medicine
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King, Benjamin R; Hershkowitz, Dylan; Eisenhauer, Philip L et al. (2017) A Map of the Arenavirus Nucleoprotein-Host Protein Interactome Reveals that Junín Virus Selectively Impairs the Antiviral Activity of Double-Stranded RNA-Activated Protein Kinase (PKR). J Virol 91:
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Ziegler, Christopher M; Eisenhauer, Philip; Bruce, Emily A et al. (2016) A novel phosphoserine motif in the LCMV matrix protein Z regulates the release of infectious virus and defective interfering particles. J Gen Virol 97:2084-9
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