ArticleJournal of cell science2023
Toxoplasma gondii scavenges mammalian host organelles through the usurpation of host ESCRT-III and Vps4A.
Article in Journal of cell science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 9 citations in OpenAlex.
- Short linear motifs-underexplored players drivingMicrobiology spectrum · 2026Article
- Article
- The parasitophorous vacuole membrane of Toxoplasma gondii: A custom structural framing with smart interior plumbing for resource allocation.PLoS pathogens · 2026Review
- Article
- TgSEC14-LTP1 is a vacuole-secreted SEC14/CRAL-TRIO-like protein required for host DAG flux and PC homeostasis in T. gondii.Cell reports · 2026Article
- 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
- CRISPR-based functional profiling of the Toxoplasma gondii genome during acute murine infection.Nature microbiology · 2024Article
- Article
- Genome-wide CRISPR screen identifies genes synthetically lethal with GRA17, a nutrient channel encoding gene in Toxoplasma.PLoS pathogens · 2023Article
- The multifaceted interactions between pathogens and host ESCRT machinery.PLoS pathogens · 2023Review
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Intracellular pathogens exploit cellular resources through host cell manipulation. Within its nonfusogenic parasitophorous vacuole (PV), Toxoplasma gondii targets host nutrient-filled organelles and sequesters them into the PV through deep invaginations of the PV membrane (PVM) that ultimately detach from this membrane. Some of these invaginations are generated by an intravacuolar network (IVN) of parasite-derived tubules attached to the PVM. Here, we examined the usurpation of host ESCRT-III and Vps4A by the parasite to create PVM buds and vesicles. CHMP4B associated with the PVM/IVN, and dominant-negative (DN) CHMP4B formed many long PVM invaginations containing CHMP4B filaments. These invaginations were shorter in IVN-deficient parasites, suggesting cooperation between the IVN and ESCRT. In infected cells expressing Vps4A-DN, enlarged intra-PV structures containing host endolysosomes accumulated, reflecting defects in PVM scission. Parasite mutants lacking T. gondii (Tg)GRA14 or TgGRA64, which interact with ESCRT, reduced CHMP4B-DN-induced PVM invaginations and intra-PV host organelles, with greater defects in a double knockout, revealing the exploitation of ESCRT to scavenge host organelles by Toxoplasma.
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Registered trials
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