Evidence map›Paper›PMID 19018990›Full record

ArticleMolecular plant pathology2008

RNA silencing-mediated resistance to a crinivirus (Closteroviridae) in cultivated sweet potato (Ipomoea batatas L.) and development of sweet potato virus disease following co-infection with a potyvirus.

Jan F Kreuze, Ilanit Samolski Klein, Milton Untiveros Lazaro, Wilmer J Cuellar Chuquiyuri, Gabriela Lajo Morgan, Patricia G Cipriani Mejía, Marc Ghislain, Jari P T Valkonen

Open access · bronzeAbstract read
In one paragraph

Article in Molecular plant pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
7.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 67 citations in OpenAlex.

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  17. Crinivirus replication and host interactions.Frontiers in microbiology · 2013
    Article
  18. Article
  19. Article
  20. Elimination of antiviral defense by viral RNase III.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 3 countries.

Jan F KreuzeInternational Potato Center (CIP), Applied Biotechnology Laboratory, Germplasm Enhancement and Crop Improvement Division, PO Box 1558, Lima 12, Peru. j.kreuze@cgiar.org
Ilanit Samolski Klein
Milton Untiveros Lazaro
Wilmer J Cuellar Chuquiyuri
Gabriela Lajo Morgan
Patricia G Cipriani Mejía
Marc Ghislain
Jari P T Valkonen
International Potato Center · PEUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sweet potato chlorotic stunt virus (SPCSV; genus Crinivirus, family Closteroviridae) is one of the most important pathogens of sweet potato (Ipomoea batatas L.). It can reduce yields by 50% by itself and cause various synergistic disease complexes when co-infecting with other viruses, including sweet potato feathery mottle virus (SPFMV; genus Potyvirus, family Potyviridae). Because no sources of true resistance to SPCSV are available in sweet potato germplasm, a pathogen-derived transgenic resistance strategy was tested as an alternative solution in this study. A Peruvian sweet potato landrace 'Huachano' was transformed with an intron-spliced hairpin construct targeting the replicase encoding sequences of SPCSV and SPFMV using an improved genetic transformation procedure with reproducible efficiency. Twenty-eight independent transgenic events were obtained in three transformation experiments using a highly virulent Agrobacterium tumefaciens strain and regeneration through embryogenesis. Molecular analysis indicated that all regenerants were transgenic, with 1-7 transgene loci. Accumulation of transgene-specific siRNA was detected in most of them. None of the transgenic events was immune to SPCSV, but ten of the 20 tested transgenic events exhibited mild or no symptoms following infection, and accumulation of SPCSV was significantly reduced. There are few previous reports of RNA silencing-mediated transgenic resistance to viruses of Closteroviridae in cultivated plants. However, the high levels of resistance to accumulation of SPCSV could not prevent development of synergistic sweet potato virus disease in those transgenic plants also infected with SPFMV.

Indexed as

Blotting, NorthernCrinivirusDNA, BacterialImmunity, InnateIpomoea batatasPlant DiseasesPlants, Genetically ModifiedPotyvirusRNA-Dependent RNA PolymeraseRNA InterferenceTransformation, GeneticDNA, BacterialRNA-Dependent RNA PolymeraseT-DNA

Identifiers

PMID19018990
PMCPMC6640417
OpenAlexW1991840340

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.