ArticlePLoS pathogens2018
Identification of a novel protein complex essential for effector translocation across the parasitophorous vacuole membrane of Toxoplasma gondii.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 124 citations in OpenAlex.
- A Suite of EightbioRxiv : the preprint server for biology · 2026Article
- Dense granule proteins: key mediators ofFrontiers in medicine · 2026Review
- Article
- An overview of the interconnectedness of the PEXEL and non-PEXEL mediated protein export iniScience · 2025Review
- Perforation of the host cell plasma membrane during Toxoplasma invasion requires rhoptry exocytosis.EMBO reports · 2025Article
- Mitochondria protect against an intracellular pathogen by restricting access to folate.Science (New York, N.Y.) · 2025Article
- Proteolytic processing and host nuclear targeting of the novel effector GRA84 inMolecular biology of the cell · 2025Article
- Toxoplasma gondii infection induces early host cell cycle arrest and DNA damage in primary human host cells by a MYR1-dependent mechanism.Communications biology · 2024Article
- Paracrine rescue of MYR1-deficienteLife · 2024Article
- Immunization with the NcMYR1 gene knockout strain effectively protected C57BL/6 mice and their pups against theVirulence · 2024Article
- CRISPR-based functional profiling of the Toxoplasma gondii genome during acute murine infection.Nature microbiology · 2024Article
- Article
- Engineering Toxoplasma gondii secretion systems for intracellular delivery of multiple large therapeutic proteins to neurons.Nature microbiology · 2024Article
- Article
- Dendritic cell-mediated responses to secreted Cryptosporidium effectors promote parasite-specific CD8Mucosal immunology · 2024Article
- Trx4, a novel thioredoxin protein, is important for Toxoplasma gondii fitness.Parasites & vectors · 2024Article
- Article
- Emergent actin flows explain distinct modes of gliding motility.Nature physics · 2024Article
- Toxoplasma protein export and effector function.Nature microbiology · 2024Review
- Subversion from Within and Without: Effector Molecule Transfer from Obligate Intracellular Apicomplexan Parasites to Human Host Cells.Results and problems in cell differentiation · 2024Review
2 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Toxoplasma gondii is an obligate intracellular parasite that can infect virtually all nucleated cells in warm-blooded animals. The ability of Toxoplasma tachyzoites to infect and successfully manipulate its host is dependent on its ability to transport "GRA" proteins that originate in unique secretory organelles called dense granules into the host cell in which they reside. GRAs have diverse roles in Toxoplasma's intracellular lifecycle, including co-opting crucial host cell functions and proteins, such as the cell cycle, c-Myc and p38 MAP kinase. Some of these GRA proteins, such as GRA16 and GRA24, are secreted into the parasitophorous vacuole (PV) within which Toxoplasma replicates and are transported across the PV membrane (PVM) into the host cell, but the translocation process and its machinery are not well understood. We previously showed that TgMYR1, which is cleaved by TgASP5 into two fragments, localizes to the PVM and is essential for GRA transport into the host cell. To identify additional proteins necessary for effector transport, we screened Toxoplasma mutants defective in c-Myc up-regulation for their ability to export GRA16 and GRA24 to the host cell nucleus. Here we report that novel proteins MYR2 and MYR3 play a crucial role in translocation of a subset of GRAs into the host cell. MYR2 and MYR3 are secreted into the PV space and co-localize with PV membranes and MYR1. Consistent with their predicted transmembrane domains, all three proteins are membrane-associated, and MYR3, but not MYR2, stably associates with MYR1, whose N- and C-terminal fragments are disulfide-linked. We further show that fusing intrinsically disordered effectors to a structured DHFR domain blocks the transport of other effectors, consistent with a translocon-based model of effector transport. Overall, these results reveal a novel complex at the PVM that is essential for effector translocation into the host cell.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.