ArticleNature microbiology2025
Toxoplasma effector TgROP1 establishes membrane contact sites with the endoplasmic reticulum during infection.
Article in Nature microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Integrated Proteomic Screening Reveals Heme Enzyme Depletion Induces Cyst-like Vacuole Formation inInternational journal of molecular sciences · 2026Article
- Short linear motifs-underexplored players drivingMicrobiology spectrum · 2026Article
- The parasitophorous vacuole membrane of Toxoplasma gondii: A custom structural framing with smart interior plumbing for resource allocation.PLoS pathogens · 2026Review
- Advancing the monitoring of organelle contact sites in vitro and in vivo.Biochemical Society transactions · 2026Review
- Dense granule proteins: key mediators ofFrontiers in medicine · 2026Review
- Toxoplasma gondii VIP1 mediates parasitophorous vacuole-host endoplasmic reticulum interactions to facilitate parasite development.Nature microbiology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors.
Funding
Abstract
Membrane contact sites (MCS) are essential for organelle communication in eukaryotic cells. Pathogens also establish MCS with host organelles, but the mechanisms underlying these interactions and their role in infection remain poorly understood. Here, using a fluorescence sensor and CRISPR-based loss-of-function screening, together with imaging and proteomics, we identify the parasite effector mediating MCS between host endoplasmic reticulum (ER) and the vacuole containing the intracellular parasite Toxoplasma gondii. TgROP1 acts as a tether and mimics a canonical FFAT motif to bind the host ER proteins VAPA and VAPB. The loss of VAPA/B abolished host ER-Toxoplasma MCS and decreased pathogen growth. These findings indicate that targeting of host MCS tethers is a strategy exploited by pathogens during infection, which could inform future treatment design.
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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.