The Toxoplasma effector TEEGR promotes parasite persistence by modulating NF-κB signalling via EZH2
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ABSTRACT:
PROVIDER: PRJNA453541 | ENA |
REPOSITORIES: ENA
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Project description:The protozoan parasite Toxoplasma gondii has co-evolved with its homeothermic hosts (humans included) strategies that drive its quasi-asymptomatic persistence in hosts, hence optimizing the chance of transmission to new hosts. Persistence, which starts with a small subset of parasites that escape host immune killing and colonize the so-called immune privileged tissues where they differentiate into a low replicating stage, is driven by the interleukin 12 (IL-12)-interferon-γ (IFN-γ) axis. Recent characterization of a family of Toxoplasma effectors that are delivered into the host cell, in which they rewire the host cell gene expression, has allowed the identification of regulators of the IL-12-IFN-γ axis, including repressors. We now report on the dense granule-resident effector, called TEEGR (Toxoplasma E2F4-associated EZH2-inducing gene regulator) that counteracts the nuclear factor-κB (NF-κB) signalling pathway. Once exported into the host cell, TEEGR ends up in the nucleus where it not only complexes with the E2F3 and E2F4 host transcription factors to induce gene expression, but also promotes shaping of a non-permissive chromatin through its capacity to switch on EZH2. Remarkably, EZH2 fosters the epigenetic silencing of a subset of NF-κB-regulated cytokines, thereby strongly contributing to the host immune equilibrium that influences the host immune response and promotes parasite persistence in mice.
2019-02-15 | GSE113626 | GEO
Project description:The protozoan parasite Toxoplasma gondii has co-evolved with its homeothermic hosts (humans included) strategies that drive its quasi-asymptomatic persistence in hosts, hence optimizing the chance of transmission to new hosts. Persistence, which starts with a small subset of parasites that escape host immune killing and colonize the so-called immune privileged tissues where they differentiate into a low replicating stage, is driven by the interleukin 12 (IL-12)-interferon-γ (IFN-γ) axis. Recent characterization of a family of Toxoplasma effectors that are delivered into the host cell, in which they rewire the host cell gene expression, has allowed the identification of regulators of the IL-12-IFN-γ axis, including repressors. We now report on the dense granule-resident effector, called TEEGR (Toxoplasma E2F4-associated EZH2-inducing gene regulator) that counteracts the nuclear factor-κB (NF-κB) signalling pathway. Once exported into the host cell, TEEGR ends up in the nucleus where it not only complexes with the E2F3 and E2F4 host transcription factors to induce gene expression, but also promotes shaping of a non-permissive chromatin through its capacity to switch on EZH2. Remarkably, EZH2 fosters the epigenetic silencing of a subset of NF-κB-regulated cytokines, thereby strongly contributing to the host immune equilibrium that influences the host immune response and promotes parasite persistence in mice.
2019-02-15 | GSE113658 | GEO
Project description:The protozoan parasite Toxoplasma gondii has co-evolved with its homeothermic hosts (humans included) strategies that drive its quasi-asymptomatic persistence in hosts, hence optimizing the chance of transmission to new hosts. Persistence, which starts with a small subset of parasites that escape host immune killing and colonize the so-called immune privileged tissues where they differentiate into a low replicating stage, is driven by the interleukin 12 (IL-12)-interferon-γ (IFN-γ) axis. Recent characterization of a family of Toxoplasma effectors that are delivered into the host cell, in which they rewire the host cell gene expression, has allowed the identification of regulators of the IL-12-IFN-γ axis, including repressors. We now report on the dense granule-resident effector, called TEEGR (Toxoplasma E2F4-associated EZH2-inducing gene regulator) that counteracts the nuclear factor-κB (NF-κB) signalling pathway. Once exported into the host cell, TEEGR ends up in the nucleus where it not only complexes with the E2F3 and E2F4 host transcription factors to induce gene expression, but also promotes shaping of a non-permissive chromatin through its capacity to switch on EZH2. Remarkably, EZH2 fosters the epigenetic silencing of a subset of NF-κB-regulated cytokines, thereby strongly contributing to the host immune equilibrium that influences the host immune response and promotes parasite persistence in mice.
2019-02-15 | GSE113618 | GEO
Project description:The Toxoplasma effector TEEGR promotes parasite persistence by modulating NF-κB signalling via EZH2
| PRJNA453540 | ENA
Project description:The Toxoplasma effector TEEGR promotes parasite persistence by modulating NF-κB signalling via EZH2
| PRJNA453543 | ENA
Project description:The Toxoplasma effector TEEGR promotes parasite persistence by modulating NF-κB signalling via EZH2
| PRJNA453541 | ENA
Project description:The protozoan parasite Toxoplasma gondii has co-evolved with its homeothermic hosts (humans included) strategies that drive its quasi-asymptomatic persistence in hosts, hence optimizing the chance of transmission to new hosts. Persistence, which starts with a small subset of parasites that escape host immune killing and colonize the so-called immune privileged tissues where they differentiate into a low replicating stage, is driven by the interleukin 12 (IL-12)-interferon-γ (IFN-γ) axis. Recent characterization of a family of Toxoplasma effectors that are delivered into the host cell, in which they rewire the host cell gene expression, has allowed the identification of regulators of the IL-12-IFN-γ axis, including repressors. We now report on the dense granule-resident effector, called TEEGR (Toxoplasma E2F4-associated EZH2-inducing gene regulator) that counteracts the nuclear factor-κB (NF-κB) signalling pathway. Once exported into the host cell, TEEGR ends up in the nucleus where it not only complexes with the E2F3 and E2F4 host transcription factors to induce gene expression, but also promotes shaping of a non-permissive chromatin through its capacity to switch on EZH2. Remarkably, EZH2 fosters the epigenetic silencing of a subset of NF-κB-regulated cytokines, thereby strongly contributing to the host immune equilibrium that influences the host immune response and promotes parasite persistence in mice.
| S-EPMC6591128 | biostudies-literature
Project description:To identify accessible chromatin regions in the human host cells during Toxoplasma parasite infection (uninfected, RH-infected and Pru-infected human foreskin fibroblasts) and in the obligate intracellular parasite Toxoplasma gondii (Type 1 RH strain and Type 2 Pru strain), ATAC-seq was performed.
2022-09-30 | GSE209866 | GEO
Project description:Parasite gene expression differences have been reported previously between RH-ERP, RH-JSR and GT1. To independently confirm these gene expression differences, we examined the parasite gene expression profiles of RH-ERP, RH-JSR and GT1 through microarray. Three type I strains of Toxoplasma gondii were compared with one array each, and these were used to verify data from previous studies.
2013-08-20 | E-GEOD-44191 | biostudies-arrayexpress
Project description:The bromdomain protein TgBDP3 is associated with the TFIID transcriptioanl initiation complex in Toxoplasma gondii. To determine the genes that are regulated by TgBDP3, the endogenous tgbdp3 locus was modified to introduce a C-terminal HA epitope tag. ChIP-seq was performed on intracellular, replicating tachyzoites expressing TgBDP3-HA. The protein was enriched in the upstream, promoter region of a subset of actively transcribed parasite genes indicating that TgBDP3 has a role in regulation of transcriptional initiation in Toxoplasma.
2023-12-18 | GSE124251 | GEO