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Host proteins interacting with T. gondii Mitochondrial Association Factor 1

ABSTRACT: This is a quantitative mass spectrometry experiment to identify host proteins that associate with the T. gondii effector protein MAF1b, which drives the association between the T. gondii vacuole and host mitochondria

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Fibroblast

SUBMITTER: Jon Boyle

LAB HEAD: Jon Boyle

PROVIDER: PXD023485 | Pride | 2021-03-06

REPOSITORIES: Pride

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			Action	DRS
	06_P107237_PIC3.raw	Raw
	07_P107243_PIC3.raw	Raw
	08_P107244_PIC4.raw	Raw
	09_P107251_PIC4.raw	Raw
	10_P107252_PIC5.raw	Raw

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Host cell subversion by Toxoplasma GRA16, a HAUSP- and PP2A-interacting protein exported to the host cell nucleus

Project description:Toxoplasma gondii multiplies inside a parasitophorous vacuole in the host cell. Several parasite proteins have been described that hijack host signaling pathways, which mostly originate from the rhoptry organelles. We report here the identification and characterization of GRA16, the first dense granule protein shown to be exported through the parasitophorous vacuole membrane and to reach the host cell nucleus. Transcriptomic analysis revealed that GRA16 positively modulates the expression of host genes involved in cell-cycle progression and the p53 tumor suppressor pathway. We show that GRA16 directly binds two host enzymes, the deubiquitinase HAUSP and the phosphatase PP2A, and that GRA16 alters p53 protein levels in a HAUSP-dependent manner and induces the nuclear translocation of the PP2A holoenzyme. Therefore GRA16 is a novel regulator of the HAUSP/p53 pathway and together with GRA15, emerge as a subfamily of new dense granule proteins exported beyond the tachyzoites-hosting vacuole to subvert the host transcriptome. Mouse bone marrow-derived macrophages (BMDM) or Human foreskin fibroblasts (HFFs) were infected with the following Toxoplasma gondii strains: - RHku80 WT versus RHku80(deltaGRA16) mutant (in BMDM) - Pruku80 WT versus Pruku80(deltaGRA16) mutant (in BMDM) - RHku80 WT versus RHku80(deltaGRA16) mutant (in HFF)

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TRIM21 innate immune detection of GBP1-positive Toxoplasma gondii is essential for host survival

Project description:Interferon gamma (IFN) is the major pro-inflammatory cytokine conferring resistance to the intracellular vacuolar pathogen Toxoplasma gondii. Autophagy along with immunity-related GTPases (IRGs), guanylate binding proteins (GBPs) and the E3 ubiquitin ligase TNF receptor-associated factor 6 (TRAF6) mediate clearance of Toxoplasma in IFN-stimulated cells. With the exception of inflammasomes, no host innate immune mediators impacting host survival have been identified at disrupted parasitophorous vacuoles. We show that IFN drives recruitment of the E3 ubiquitin ligase TRIM21 to GBP1-positive avirulent Toxoplasma vacuoles. This led to Lys63-linked ubiquitination of the vacuole and secretion of pro-inflammatory cytokines. GBPs were ubiquitinated during infection and TRIM21 controlled their expression levels and the efficient recruitment of GBP1 to the vacuole. TRIM21 deficiency led to an enhanced early replication of Toxoplasma without interfering with vacuolar disruption. TRIM21-/- mice were highly susceptible to Toxoplasma infection, exhibiting decreased levels of pro-inflammatory cytokines and higher parasite burden in the brain. This study identifies TRIM21 as a previously unknown modulator of Toxoplasma gondii resistance thereby extending host innate immune recognition of eukaryotic pathogens to include E3 ubiquitin ligases.

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Divergent co-transcriptomes of different host cells infected with Toxoplasma gondii reveal cell type-specific host-parasite interactions

Project description:The apicomplexan parasite Toxoplasma gondii infects a broad range of different cell types in avian and mammalian hosts including humans. Infection of immunocompetent hosts is mostly asymptomatic or benign, but leads to development of largely dormant bradyzoites that persist for the hosts life predominantly within neurons and muscle cells. Here we have analyzed the impact of the host cell type on the co-transcriptomes of host and parasite using high-throughput RNA sequencing. Murine cortical neurons and astrocytes, skeletal muscle cells (SkMCs) and fibroblasts differed by more than 16,200 differentially expressed genes (DEGs) before and at 24 hours after infection with T. gondii. However, only 157 to 492 of these DEGs were regulated within the different cell types by infection. Intriguingly, largely diverse sets of genes were regulated in neurons, SkMCs, astrocytes and fibroblasts following infection indicating host cell type-specific transcriptional responses. Only a few genes were identified that were commonly regulated in two or three host cell types after infection. The heterogeneous transcriptomes of the host cells before and during infection coincided with the differential expression of ~5,400 genes in T. gondii residing in the different host cells. Expression of these DEGs mostly differed quantitatively but within neurons, T. gondii also expressed 121 genes in a strictly host cell-type specific manner. Interestingly, we identified gene clusters in both T. gondii and its host, which correlated with the predominant parasite persistence in neurons or SkMCs as compared to astrocytes or fibroblasts. Thus, heterogeneous expression profiles of different host cell types and the parasites’ ability to adapt to them may govern the parasite-host cell interaction during toxoplasmosis.

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