ArticleNature microbiology2026
Phytophthora targets plant extracellular vesicles to promote infection.
Article in Nature microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
1 citing paper in PubMed.
- Progress, Challenges, and Standardization Pathways in the Isolation and Purification Techniques of Plant-Derived Vesicles.Plants (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Extracellular vesicles (EVs) transport biologically active molecules and are known to mediate host defence against microbial pathogens, including plant fungal pathogens. However, the mechanism by which pathogens disrupt EV-dependent defence remains unclear. Here we show that Phytophthora capsici, a global crop pathogen, counteracts EV-mediated plant defence through targeted lipase activity. We show that Arabidopsis releases EVs containing tetraspanin (TET), specifically TET8- and TET9-EVs, which damage germinated spores of Phytophthora, reducing infection. As a counter-defence, Phytophthora secretes an infection-induced apoplastic lipase, Plant Extracellular Vesicle Destroyer 1 (PED1), which targets TET8- and TET9-EVs. This occurs via interaction with the EV membrane-localized protein Defective Glycosylation 1 (DGL1), which directly interacts and co-localizes with TET8 and TET9 on the EV membrane. PED1 damages TET8- and TET9-EVs through its lipase activity towards campesteryl esters, suppressing EV-mediated plant defence. Our study reveals a mechanism used by Phytophthora to counteract EV-mediated host defence.
Indexed as
Identifiers
42009757What Socratic holds
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 Socratic graph.