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Effect of BFD2 (TGME49_311100) deletion on gene expression in Toxoplasma gondii

ABSTRACT: The acute-to-chronic stage transition in Toxoplasma gondii involes a global restructuring of the parasite transcriptome and is induced under alkaline stress. We found that parasites lacking the RNA-binding protein BFD2 are unable to produce chronic forms, consistent with a block in this develomental program. To understand how BFD2 facilitates chronic-stage transcriptional reprogramming in T. gondii, we profiled the transcriptomes of both 'wildtype' and BFD2-knockout parasites under alkaline-stressed and standard culture conditions

ORGANISM(S): Toxoplasma gondii

PROVIDER: GSE223869 | GEO | 2023/03/31

REPOSITORIES: GEO

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Characterization of the BFD2-bound transcriptome in chronic-stage T. gondii

Project description:The acute-to-chronic stage transition in Toxoplasma gondii involes a global restructuring of the parasite transcriptome and can be induced by alkaline stress. Prior work identified the master regulator of this process: a MYB-like transcription factor named BFD1 that is specifically induced under stress and is both necessary and sufficient to drive differentiation. Recently, we found that parasites lacking a CCCH-type zinc finger RNA-binding protein (BFD2) are also unable to produce chronic forms due to an inability to robustly express BFD1. To test whether the influence of BFD2 on BFD1 expression involves interaction with this or other transcripts, we performed BFD2 immunoprecipitation and sequencing (RIP-seq) under alkaline stress.

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Translation initiation factor eIF1.2 orchestrates Toxoplasma gondii differentiation by regulating stage-specific gene expression

Project description:Toxoplasma gondii persists in humans by converting from actively replicating acute stage tachyzoites to slow-growing chronic stage bradyzoites. The molecular mechanisms that mediate T. gondii differentiation remain poorly understood. Through a chemical mutagenesis screen, we identified translation initiation factor eIF1.2 as being critical for T. gondii differentiation. The presence of an F97L mutation in eIF1.2 identified in the screen or the complete lack eIF1.2 (∆eIF1.2) markedly impeded bradyzoite cyst formation in culture and in the brains of infected mice. ∆eIF1.2 parasites were defective in the upregulation of bradyzoite differentiation regulators BFD1 and BFD2 during stress-induced differentiation. Conditional overexpression of BFD1 or BFD2 rescued differentiation in ∆eIF1.2 parasites. We further show that eiF1.2 interacted with the yeast 40S ribosome and directed the scanning of a model 5’ untranslated region. Together, our findings imply that eIF1.2 functions by regulating the translation of key differentiation factors necessary to establish T. gondii chronic infection.

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Project description:Successful infection strategies must balance pathogen amplification and persistence. In Toxoplasma gondii, this is accomplished through differentiation into dedicated cyst-forming chronic stages that avoid clearance by the host immune system. The transcription factor BFD1 is both necessary and sufficient for stage conversion; however, its regulation is not understood. We examine five factors transcriptionally activated by BFD1. One of these is a cytosolic RNA-binding protein of the CCCH-type zinc finger family, which we name BFD2. Parasites lacking BFD2 fail to induce BFD1 and are consequently unable to fully differentiate in culture or in mice. BFD2 interacts with the BFD1 transcript under stress and deletion of BFD2 reduces BFD1 protein levels, but not mRNA abundance. The reciprocal effects on BFD2 transcription and BFD1 translation outline a positive feedback loop that enforces commitment to differentiation. BFD2 helps explain how parasites commit to the chronic gene-expression program and elucidates how the balance between proliferation and persistence is achieved over the course of infection.

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Expression data from Toxoplasma gondii mutants and wild-type during bradyzoite differentiation in vitro

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Expression data from Toxoplasma gondii mutants and wild-type during bradyzoite differentiation in vitro

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Toxoplasma gondii lysine acetyltransferase GCN5-A functions in the cellular response to alkaline stress and expression of cyst genes

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2011-05-25 | E-GEOD-22100 | biostudies-arrayexpress

Expression data from Toxoplasma gondii mutants and wild-type during bradyzoite differentiation in vitro

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2010-07-27 | E-GEOD-23174 | biostudies-arrayexpress

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