Evidence map›Paper›PMID 25845019›Full record

ArticlePloS one2015

Necrotrophic effector epistasis in the Pyrenophora tritici-repentis-wheat interaction.

Viola A Manning, Lynda M Ciuffetti

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
8.3field-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

16 citing papers in PubMed, 41 citations in OpenAlex.

  1. Genome-wide association mapping of tan spot resistance in a modified NAM population derived from synthetic hexaploid wheat.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Effectors of Plant Necrotrophic Fungi.Frontiers in plant science · 2021
    Review
  7. Genome-wide association mapping of tan spot resistance in a worldwide collection of durum wheat.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2020
    Article
  8. Article
  9. Characterizing Virulence of thePathogens (Basel, Switzerland) · 2018
    Article
  10. Article
  11. Inverse gene-for-gene interactions contribute additively to tan spot susceptibility in wheat.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2017
    Article
  12. Review
  13. A functionally conserved ZnMolecular plant pathology · 2017
    Article
  14. Article
  15. Differential effector gene expression underpins epistasis in a plant fungal disease.The Plant journal : for cell and molecular biology · 2016
    Article
  16. 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

2 authors at 1 institution in 1 country.

Viola A ManningDepartment of Botany and Plant Pathology, Oregon State University, Corvallis, Oregon, United States of America.
Lynda M CiuffettiDepartment of Botany and Plant Pathology, Oregon State University, Corvallis, Oregon, United States of America; Center for Genome Research and Biocomputing, Oregon State University, Corvallis, Oregon, United States of America.
Oregon State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pyrenophora tritici-repentis, the causal agent of tan spot disease of wheat, mediates disease by the production of host-selective toxins (HST). The known toxins are recognized in an 'inverse' gene-for-gene manner, where each is perceived by the product of a unique locus in the host and recognition leads to disease susceptibility. Given the importance of HSTs in disease development, we would predict that the loss of any of these major pathogenicity factors would result in reduced virulence and disease development. However, after either deletion of the gene encoding the HST ToxA or, reciprocally, heterologous expression of ToxA in a race that does not normally produce the toxin followed by inoculation of ToxA-sensitive and insensitive wheat cultivars, we demonstrate that ToxA symptom development can be epistatic to other HST-induced symptoms. ToxA epistasis on certain ToxA-sensitive wheat cultivars leads to genotype-specific increases in total leaf area affected by disease. These data indicate a complex interplay between host responses to HSTs in some genotypes and underscore the challenge of identifying additional HSTs whose activity may be masked by other toxins. Also, through mycelial staining, we acquire preliminary evidence that ToxA may provide additional benefits to fungal growth in planta in the absence of its cognate recognition partner in the host.

Indexed as

Epistasis, GeneticAscomycotaFungal ProteinsGene DeletionGene Knockout TechniquesHost-Pathogen InteractionsMycotoxinsPlant DiseasesPlant LeavesTriticumFungal ProteinsMycotoxinsTOXA protein, Pyrenophora tritici-repentis

Identifiers

PMID25845019
PMCPMC4386829
OpenAlexW2045007109

What OpenQuestion holds

Textmetadata
LicenceCC0
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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.