Evidence map›Paper›PMID 24299004›Full record

ArticleMolecular plant pathology2014

Functional characterization of the mutations in Pepper mild mottle virus overcoming tomato tm-1-mediated resistance.

Hiroyuki Mizumoto, Yukino Morikawa, Kazuhiro Ishibashi, Kentaro Kimura, Kohei Matsumoto, Masayuki Tokunaga, Akinori Kiba, Masayuki Ishikawa, Tetsuro Okuno, Yasufumi Hikichi

Open access · bronzeAbstract read
In one paragraph

Article in Molecular plant pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 92% 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

0 citing papers in PubMed, 5 citations in OpenAlex.

No citing paper in PubMed yet.

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

10 authors at 3 institutions in 1 country.

Hiroyuki MizumotoLaboratory of Plant Pathology and Biotechnology, Kochi University, Nankoku, Kochi, 783-8502, Japan.
Yukino Morikawa
Kazuhiro Ishibashi
Kentaro Kimura
Kohei Matsumoto
Masayuki Tokunaga
Akinori Kiba
Masayuki Ishikawa
Tetsuro Okuno
Yasufumi Hikichi
Kōchi University · JPInstitute of Agrobiological Sciences · JPKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In tomato plants, Pepper mild mottle virus (PMMoV) cannot replicate because the tm-1 protein inhibits RNA replication. The resistance of tomato plants to PMMoV remains durable both in the field and under laboratory conditions. In this study, we constructed several mutant PMMoVs and analysed their abilities to replicate in tomato protoplasts and plants. We found that two mutants, PMMoV-899R,F976Y and PMMoV-899R,F976Y,D1098N, were able to replicate in tomato protoplasts, but only PMMoV-899R,F976Y,D1098N was able to multiply in tomato plants. Further analysis showed that the D1098N mutation of the replication proteins weakened the inhibitory effect of the tm-1 protein and enhanced the replication efficiency of PMMoV-899R,F976Y,D1098N. We also observed that the infectivity of the viruses decreased in the order wild-type PMMoV > PMMoV-899R,F976Y > PMMoV-899R,F976Y,D1098N in original host plants, pepper and tobacco plants. On the contrary, the single mutation D1098N abolished PMMoV replication in tobacco protoplasts. On the basis of these observations, it is likely that the deleterious side-effects of mutations in replication proteins prevent the emergence of PMMoV mutants that can overcome tm-1-mediated resistance.

Indexed as

MutationPlant DiseasesSolanum lycopersicumTobamovirusVirulence130 K proteinnonhostPepper mild mottle virustm-1Tobamovirustomato

Identifiers

PMID24299004
PMCPMC6638807
OpenAlexW1907556158

What OpenQuestion holds

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Registered trials

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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.