ArticleScientific reports2017
Deficiency of the eIF4E isoform nCBP limits the cell-to-cell movement of a plant virus encoding triple-gene-block proteins in Arabidopsis thaliana.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Molecular gatekeepers: eukaryotic translation factors decoding plant-virus dynamics for resistance engineering.Stress biology · 2026Review
- Broadening Virus Resistance Through Gene Pyramiding of eIF4E Family Members.Molecular plant pathology · 2025Article
- Adaptation of turnip mosaic virus toVirus evolution · 2024Article
- Interaction of EXA1 and eIF4E Family Members Facilitates Potexvirus Infection in Arabidopsis thaliana.Journal of virology · 2023Article
- Inactivation of RPX1 in Arabidopsis confers resistance to Plutella xylostella through the accumulation of the homoterpene DMNT.Plant, cell & environment · 2023Article
- Plant eIF4E isoforms as factors of susceptibility and resistance to potyviruses.Frontiers in plant science · 2023Review
- Plantago asiatica mosaic virus: An emerging plant virus causing necrosis in lilies and a new model RNA virus for molecular research.Molecular plant pathology · 2022Review
- Short 5' Untranslated Region Enables Optimal Translation of Plant Virus Tricistronic RNA via Leaky Scanning.Journal of virology · 2022Article
- Cymbidium Mosaic Virus Infecting Orchids: What, How, and What Next?Iranian journal of biotechnology · 2022Article
- Eukaryotic translation initiation factor 4E family member nCBP facilitates the accumulation of TGB-encoding viruses by recognizing the viral coat protein in potato and tobacco.Frontiers in plant science · 2022Article
- Susceptibility factor StEXA1 interacts with StnCBP to facilitate potato virus Y accumulation through the stress granule-dependent RNA regulatory pathway in potato.Horticulture research · 2022Article
- Resistance induction based on the understanding of molecular interactions between plant viruses and host plants.Virology journal · 2021Review
- Article
- Functional conservation of EXA1 among diverse plant species for the infection by a family of plant viruses.Scientific reports · 2019Article
- Site-specific manipulation of Arabidopsis loci using CRISPR-Cas9 SunTag systems.Nature communications · 2019Article
- Simultaneous CRISPR/Cas9-mediated editing of cassava eIF4E isoforms nCBP-1 and nCBP-2 reduces cassava brown streak disease symptom severity and incidence.Plant biotechnology journal · 2019Article
- Manipulating Cellular Factors to Combat Viruses: A Case Study From the Plant Eukaryotic Translation Initiation Factors eIF4.Frontiers in microbiology · 2019Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the important antiviral genetic strategies used in crop breeding is recessive resistance. Two eukaryotic translation initiation factor 4E family genes, eIF4E and eIFiso4E, are the most common recessive resistance genes whose absence inhibits infection by plant viruses in Potyviridae, Carmovirus, and Cucumovirus. Here, we show that another eIF4E family gene, nCBP, acts as a novel recessive resistance gene in Arabidopsis thaliana toward plant viruses in Alpha- and Betaflexiviridae. We found that infection by Plantago asiatica mosaic virus (PlAMV), a potexvirus, was delayed in ncbp mutants of A. thaliana. Virus replication efficiency did not differ between an ncbp mutant and a wild type plant in single cells, but viral cell-to-cell movement was significantly delayed in the ncbp mutant. Furthermore, the accumulation of triple-gene-block protein 2 (TGB2) and TGB3, the movement proteins of potexviruses, decreased in the ncbp mutant. Inoculation experiments with several viruses showed that the accumulation of viruses encoding TGBs in their genomes decreased in the ncbp mutant. These results indicate that nCBP is a novel member of the eIF4E family recessive resistance genes whose loss impairs viral cell-to-cell movement by inhibiting the efficient accumulation of TGB2 and TGB3.
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