A novel nuclear protein complex controlling the expression of developmentally regulated genes in Toxoplasma gondii [RNA-seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Toxoplasma gondii
PROVIDER: GSE277550 | GEO | 2024/12/19
REPOSITORIES: GEO
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Project description:The Toxoplasma gondii G1 RESTRICTION checkpoint operates the switch between parasite growth and differentiation. The Cdk-related G1 kinase TgCrk2 forms alternative complexes with atypical cyclins (TgCycP1, TgCycP2 and TgCyc5) in the rapidly dividing developmentally incompetent RH and slower dividing developmentally competent ME49 tachyzoites and bradyzoites. The TgCycP1 expression interferes with bradyzoite differentiation. The TgCycP2 regulates G1 in the developmentally competent ME49 but not in the developmentally incompetent RH tachyzoites. Examination of TgCycP2 and TgCyc5 in alkaline induced and spontaneous bradyzoite differentiation (rat embryonic brain cells) models confirmed TgCycP2 role in bradyzoite replication and revealed that stress induced TgCyc5 is critical for efficient tissue cyst maturation.
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Project description:Two samples, 0hr and 72hr, were used to generate tachyzoite and bradyzoite transcriptional data from tissue-cultured Toxoplasma gondii strain Prugniaud, respectively.
2010-06-15 | GSE22258 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE11437: Expression QTL mapping of Toxoplasma gondii genes, Bradyzoite array GSE11514: Expression QTL mapping of Toxoplasma gondii genes, Tachyzoite array Keywords: SuperSeries Refer to individual Series
2008-05-22 | E-GEOD-11515 | biostudies-arrayexpress
Project description:Toxoplasma gondii is an intracellular parasitic protozoan that poses a significant risk to pregnant women and immunocompromised individuals. T. gondii tachyzoites duplicate rapidly in host cells during acute infection through endodyogeny. This highly regulated division process is accompanied by complex gene regulation networks. TgAP2XII-9 is a cyclical transcription factor, but its specific role in the parasite cell cycle is not fully understood. Here, we demonstrate that TgAP2XII-9 is identified as a nuclear transcription factor and is dominantly expressed during the S/M phase of the tachyzoite cell cycle. CUT&Tag results indicate that TgAP2XII-9 targets key genes for the moving junction machinery (RON2, 4, 8) and daughter cell inner membrane complex (IMC). TgAP2XII-9 deficiency resulted in a significant downregulation of rhoptry proteins and rhoptry neck proteins, leading to a severe defect in the invasion and egress efficiency of tachyzoites. Additionally, the loss of TgAP2XII-9 correlated with a substantial downregulation of multiple IMC and apicoplast proteins, leading to disorders of daughter bud formation and apicoplast inheritance, and further contributing to the inability of cell division and intracellular proliferation. Our study reveals that TgAP2XII-9 acts as a critical S/M-phase regulator that orchestrates the endodyogeny and apicoplast division in T. gondii tachyzoite. This study contributes to a broader understanding of the complexity of the parasite’s cell cycle and its key regulators.
2024-05-05 | GSE266204 | GEO
Project description:To investigate transcriptional role of TgAP2XII-1 on type II Toxoplasma gondii (ME49 Tir1), an auxin inducible degron system was introduced to control the protein expression of TgAP2XII-1 and the target protein could be totally degradated in 3h after adding IAA.
2023-05-01 | GSE228580 | GEO
Project description:Two samples, 0hr and 72hr, were used to generate tachyzoite and bradyzoite transcriptional data from tissue-cultured Toxoplasma gondii strain Prugniaud, respectively. Samples are single replicates, and a subset of a larger timeseries. Non-control sample was exposed to alkaline conditions, media pH 8.2, for 72hr.
2010-06-15 | E-GEOD-22258 | biostudies-arrayexpress
Project description:Toxoplasma gondii pathogenesis includes the invasion of host cells by extracellular parasites (tachyzoites), replication of intracellular tachyzoites, and differentiation to a latent bradyzoite stage. Whole genome expression profiling was carried out using the newly developed Affymetrix ToxoGeneChip (GeneChip Tgondiia520372) in order to analyze the ~8,000 predicted genes in the T. gondii genome of mutants and wild-type, allowing for full-scale expression profiling during bradyzoite differentiation in vitro.
2010-07-27 | GSE23174 | GEO
Project description:Toxoplasma has been a useful parasite model for decades because it is relatively easy to genetically modify and culture, however, attempts to generate and study the recrudescence of tissue cysts have come up short with lab-adapted strains generating low numbers of tissue cysts in vivo. Here we have established a new model of Toxoplasma recrudescence using bradyzoites from an unadapted Type II ME49 strain (ME49EW) isolated from murine brain tissue. Ex vivo bradyzoite infection of fibroblasts and astrocytes produced sequential tachyzoite growth stages; a fast-growing stage was followed by formation of a slower-growing stage. In astrocytes, but not in fibroblasts, bradyzoites also initiated a second recrudescent pathway involving bradyzoite to bradyzoite replication. Intraperitoneal infections of mice with either bradyzoites or the fast-growing tachyzoite stage efficiently disseminated to brain tissue leading to high numbers of tissue cysts, while infections with the slow-growing tachyzoite stage were largely retained in the peritoneum. Poor infection and cyst formation of slow-growing tachyzoites was reversible by serial tissue cyst passage, while the poor tissue cyst formation of lab-adapted tachyzoites was not reversible by these approaches. To distinguish strain developmental competency, we identified Toxoplasma genes highly expressed in ME49EW in vivo tissue cysts and developed a qPCR approach that differentiates immature from mature bradyzoites. In summary, the results presented describe a new ex vivo bradyzoite recrudescence model that fully captures the growth and developmental processes during toxoplasmosis reactivation in vivo opening the door to the further study of these important features of the Toxoplasma intermediate life cycle.
2022-07-23 | GSE208647 | GEO
Project description:Ingestion of Toxoplasma gondii results in life-long infection due to its ability to convert from the rapidly disseminating tachyzoite stage to the chronic, encysted bradyzoite stage. The control of mRNA translation has been suggested to play a key role in the signaling required to trigger bradyzoite formation. In eukaryotes, translational control primarily operates at two key points during the assembly of translation initiation factors. The phosphorylation of eIF2 affects mRNA start codon recognition and promotes differentiation in a variety of parasites. Modulating eIF4F function is the second pan-eukaryote regulatory point but remains unexplored in Toxoplasma. Here, we uncover the role that eIF4F-centric regulation plays in regulating bradyzoite formation by targeting the cap-binding subunit, eIF4E1. We discover that eIF4E1 coordinates two eIF4F complexes and binds the 5’-end of all mRNAs transcribed in tachyzoites, many of which show evidence of stemming from heterogenous transcriptional start sites. Together, this indicates that eIF4E1 is the predominant cap-binding protein in Toxoplasma tachyzoites. We also demonstrate that eIF4E1 knockdown or its chemical inhibition triggers the efficient formation of bradyzoites in the absence of other stresses and that stress-induced bradyzoites reduce their eIF4E1 expression. This study unearths a role for eIF4F-centric translational control in controlling Toxoplasma differentiation, suggesting that control of cap-dependent translation regulates the process of bradyzoite formation.
2023-11-02 | GSE243206 | GEO
Project description:Ingestion of Toxoplasma gondii results in life-long infection due to its ability to convert from the rapidly disseminating tachyzoite stage to the chronic, encysted bradyzoite stage. The control of mRNA translation has been suggested to play a key role in the signaling required to trigger bradyzoite formation. In eukaryotes, translational control primarily operates at two key points during the assembly of translation initiation factors. The phosphorylation of eIF2 affects mRNA start codon recognition and promotes differentiation in a variety of parasites. Modulating eIF4F function is the second pan-eukaryote regulatory point but remains unexplored in Toxoplasma. Here, we uncover the role that eIF4F-centric regulation plays in regulating bradyzoite formation by targeting the cap-binding subunit, eIF4E1. We discover that eIF4E1 coordinates two eIF4F complexes and binds the 5’-end of all mRNAs transcribed in tachyzoites, many of which show evidence of stemming from heterogenous transcriptional start sites. Together, this indicates that eIF4E1 is the predominant cap-binding protein in Toxoplasma tachyzoites. We also demonstrate that eIF4E1 knockdown or its chemical inhibition triggers the efficient formation of bradyzoites in the absence of other stresses and that stress-induced bradyzoites reduce their eIF4E1 expression. This study unearths a role for eIF4F-centric translational control in controlling Toxoplasma differentiation, suggesting that control of cap-dependent translation regulates the process of bradyzoite formation.
2023-11-02 | GSE243203 | GEO