CHARACTERIZATION OF THE DISRUPTED LOCUS IN A TOXOPLASMA GONDII BRADYZOITE DIFFER

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The human pathogen Toxoplasma gondii is one of the most widely distributed protozoan parasites, infecting approximately one-third of the world?s population. Two forms characterize asexual reproduction of T. gondii; rapidly growing ?tachyzoites? and latent ?bradyzoite? tissue cysts. These two developmental stages are central to disease propagation and causation. The interconversion between tachyzoites and bradyzoites, at the heart of parasite survival and pathogenicity, is poorly understood at a molecular and genetic level, which makes understanding this process an important goal. Recently, a genetic screen was developed to identify regulatory genes that control parasite differentiation and mutants that fail to convert to bradyzoites under differentiation conditions have been isolated. The disrupted locus in one of these mutants (mutant B7) has been identified and the expression of a developmentally regulated transcript (B41) has been abolished in the mutant parasites. B41 is transcribed; yet it contains no obvious open reading frame. The goal of this project is to functionally characterize the disrupted locus in the mutant B7 and test the hypothesis that this locus codes for a functional non-coding RNA that plays a critical role in bradyzoite formation.