ArticleViruses2016
The p22 RNA Silencing Suppressor of the Crinivirus Tomato chlorosis virus is Dispensable for Local Viral Replication but Important for Counteracting an Antiviral RDR6-Mediated Response during Systemic Infection.
Article in Viruses, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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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.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Chloroplast Fibrillin-Mediated α-Tocopherol Biosynthesis Impaired by a Virus to Enhance Infection and to Improve Drought Tolerance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Tomato chlorosis virus p22 interacts with NbBAG5 to inhibit autophagy and regulate virus infection.Molecular plant pathology · 2023Article
- Small RNAs Participate in Plant-Virus Interaction and Their Application in Plant Viral Defense.International journal of molecular sciences · 2022Review
- Influence of virus-host interactions on plant response to abiotic stress.Plant cell reports · 2021Review
- Cucumber Ribosomal Protein CsRPS21 Interacts With P22 Protein of Cucurbit Chlorotic Yellows Virus.Frontiers in microbiology · 2021Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Among the components of the RNA silencing pathway in plants, RNA-dependent RNA polymerases (RDRs) play fundamental roles in antiviral defence. Here, we demonstrate that the Nicotiana benthamiana RDR6 is involved in defence against the bipartite crinivirus (genus Crinivirus, family Closteroviridae) Tomato chlorosis virus (ToCV). Additionally, by producing a p22-deficient ToCV infectious mutant clone (ToCVΔp22), we studied the role of this viral suppressor of RNA silencing in viral infection in both wild-type and RDR6-silenced N. benthamiana (NbRDR6i) plants. We demonstrate that p22 is dispensable for the replication of ToCV, where RDR6 appears not to have any effect. Furthermore, the finding that ToCV∆p22 systemic accumulation was impaired in wild-type N. benthamiana but not in NbRDR6i plants suggests a role for p22 in counteracting an RDR6-mediated antiviral response of the plant during systemic infection.
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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.