ArticleScience advances2026
A viral protein diverts the endocytic VPS9a-Rab5 pathway to promote virus infection in plants.
Article in Science advances, 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.
- The Small GTPase RHO1 Regulates ROS Homeostasis and Differentially Responds to Pathogens Infection via Interaction With Aquaporin TIP1;1 in Nicotiana.Molecular plant pathology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endocytosis is central to cellular trafficking and signaling across eukaryotes, yet whether and how plant viruses actively reprogram this pathway remains unclear. Here, we show that the geminiviral betasatellite-encoded βC1 reprograms the host VPS9a-Rab5 endocytic module to promote viral infection. βC1 associates with the Rab5 GTPases ARA6 and ARA7 as well as their guanine nucleotide exchange factor VPS9a, stabilizing the VPS9a-Rab5 complex and enhancing nucleotide exchange. This catalytic potentiation sustains Rab5 activation and drives endosome proliferation, which, in turn, stabilizes βC1 to support efficient viral replication. Genetic disruption of Rab5 or VPS9a compromises endocytosis, reduces βC1 accumulation, and restricts infection by multiple geminiviruses. Together, these findings define the VPS9a-Rab5 module as a central proviral hub linking host membrane dynamics to effector stability and viral DNA amplification, revealing an unanticipated strategy in which a viral effector amplifies a cellular regulatory catalyst to reprogram a fundamental cellular pathway for virus infection.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.