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Effect of depleting BFD1-regulated gene-expression factors (TGME49_253790, TGME49_208020, TGME49_224630, TGME49_306620, TGME49_311100) on the Toxoplasma transcriptome during alkaline stress

ABSTRACT: Effect of depleting BFD1-regulated gene-expression factors (TGME49_253790, TGME49_208020, TGME49_224630, TGME49_306620, TGME49_311100) on the Toxoplasma transcriptome during alkaline stress

PROVIDER: PRJNA928461 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23248134_1.fastq.gz	Fastqsanger.gz
	SRR23248134_2.fastq.gz	Fastqsanger.gz
	SRR23248135_1.fastq.gz	Fastqsanger.gz
	SRR23248135_2.fastq.gz	Fastqsanger.gz
	SRR23248136_1.fastq.gz	Fastqsanger.gz

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Effect of depleting BFD1-regulated gene-expression factors (TGME49_253790, TGME49_208020, TGME49_224630, TGME49_306620, TGME49_311100) on the Toxoplasma transcriptome during alkaline stress

Project description:The transcription factor BFD1 is the master regulator of the Toxoplasma chronic-stage differentiation program, which is induced under alkaline stress. Prior work indicated that BFD1 transcriptionally activates five other putative RNA- and DNA-binding proteins during differentiation, suggesting potential secondary roles in shaping the Toxoplasma chronic-stage transcriptome. To describe the distinct genetic cohorts controlled by these factors, we generated individual knockdown strains for each candidate using the auxin inducible degron system (TIR1/AID) and examined the transcriptomic effects of their depletion under alkaline stress.

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CUT&RUN profiling of genomic BFD1 binding sites

Project description:Using an epitope-tagged BFD1-complemented strain, the genomic binding of BFD1 was assessed in alkaline-stress induced bradyzoites.

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RNA-sequencing of parasites overexpressing conditionally stabilized BFD1 to identify genes regulated by BFD1

Project description:WT (ME49∆KU80), ∆BFD1, or ∆BFD1/DD-BFD1-Ty parasites were treated with the stabilizing ligand Shield-1 (all three) or vehicle alone (WT and ∆BFD1/DD-BFD1-Ty) to identify genes differentially regulated by overexpression of BFD1.

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Effects of BFD1 (TGME49_200385) and BFD2 (TGME49_311100) deletion on gene expression in Toxoplasma gondii during infection in neurons

Project description:Differentiation of proliferative acute stages into semi-quiescent chronic stages is key for Toxoplasma gondii persistence within an infected host. During natural infection, chronic stages are almost exclusively found in neurons, and it is well appreciated that neurons support high rates of spontaneous differentiation in cell culture. Recently, 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 compare the effects of BFD1 and BFD2 on chronic-stage transcriptional reprogramming in T. gondii, we profiled the transcriptomes of both 'wildtype' and BFD1- and BFD2-knockout parasites during infection of murine primary neurons.

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Effect of BFD2 (TGME49_311100) knockout on T. gondii gene expression during BFD1 induction

Project description:The acute-to-chronic stage transition in Toxoplasma gondii involes a global restructuring of the parasite transcriptome. Prior work identified a single transcription factor (BFD1) that is both necessary and sufficient to establish the chronic-stage program, making it the master regulator of this process. Recently, we found that parasites lacking a CCCH-type zinc finger RNA-binding protein (BFD2) are also unable to produce chronic forms. To understand how BFD2 aids in establishing the BFD1 transcriptional program, we knocked out BFD2 in a BFD1-conditional expression strain, wherein BFD1 is induced by treatment with the small molecule Shield-1.

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

Project description:Parasitic protozoa such as the apicomplexan Toxoplasma gondii progress through their life cycle in response to stimuli in the environment or host organism. Very little is known about how proliferating tachyzoites reprogram their expressed genome in response to stresses that prompt development into latent bradyzoite cysts. We have previously linked histone acetylation with the expression of stage-specific genes, but the factors involved remain to be determined. We sought to determine if GCN5, which operates as a transcriptional co-activator by virtue of its histone acetyltransferase (HAT) activity, contributed to stress-induced changes in gene expression in Toxoplasma. In contrast to other lower eukaryotes, Toxoplasma has duplicated its GCN5 lysine acetyltransferase (KAT). Disruption of the gene encoding for TgGCN5-A did not produce a severe phenotype under normal culture conditions, but here we show that the TgGCN5-A null mutant is deficient in recovering from alkaline pH, a common stress used to induce bradyzoite differentiation in vitro. The TgGCN5-A knockout is incapable of up-regulating key marker genes expressed during development of the latent cyst form. Complementation of the TgGCN5-A knockout restores the expression of these stress-induced genes and reverses the stress recovery defect. We also describe a genome-wide analysis of the Toxoplasma transcriptional response to alkaline pH stress, finding that TgGCN5-A knockout parasites fail to up-regulate 68% of the stress response genes that are induced 2-fold or more in wild-type. Using chromatin immunoprecipitation, we verify an enrichment of TgGCN5-A at the upstream regions of genes activated by alkaline pH exposure, including developmentally regulated genes. Wild-type and GCN5-A- Knockout organisms were subjected to control and stress treatments

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

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

2011-05-25 | GSE22100 | GEO

Transcriptome analysis of Toxoplasma gondii BFD1 deletion mutants in low iron conditions

Project description:Transcriptome analysis of Toxoplasma gondii BFD1 deletion mutants in low iron conditions

| PRJEB83013 | ENA

A positive feedback loop controls Toxoplasma chronic differentiation

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.

2023-08-07 | PXD039648 | Pride

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