Evidence map›Paper›PMID 20084492›Full record

ArticleTAG. Theoretical and applied genetics. Theoretische und angewandte Genetik2010

Genetic analysis of disease susceptibility contributed by the compatible Tsn1-SnToxA and Snn1-SnTox1 interactions in the wheat-Stagonospora nodorum pathosystem.

C-G Chu, J D Faris, S S Xu, Timothy L Friesen

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Article in TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.0field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Assessing European Wheat Sensitivities toFrontiers in plant science · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. Article
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  14. Article
  15. New broad-spectrum resistance to septoria tritici blotch derived from synthetic hexaploid wheat.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2012
    Article
  16. Genetic analysis of resistance to septoria tritici blotch in the French winter wheat cultivars Balance and Apache.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2011
    Article
  17. 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

4 authors at 3 institutions in 1 country.

C-G ChuDepartment of Plant Sciences, North Dakota State University, Fargo, ND, 58105, USA.
J D Faris
S S Xu
Timothy L Friesen
Agricultural Research Service · USEdward T. Schafer Agricultural Research Center · USNorth Dakota State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stagonospora nodorum is a foliar pathogen of wheat that produces several host-selective toxins (HSTs) and causes the disease Stagonospora nodorum blotch (SNB). The wheat genes Snn1 and Tsn1 confer sensitivity to the HSTs SnTox1 and SnToxA, respectively. The objectives of this study were to dissect, quantify, and compare the effects of compatible Snn1-SnTox1 and Tsn1-SnToxA interactions on susceptibility in the wheat-S. nodorum pathosystem. Inoculation of a wheat doubled haploid population that segregates for both Snn1 and Tsn1 with an S. nodorum isolate that produces both SnTox1 and SnToxA indicated that both interactions were strongly associated with SNB susceptibility. The Snn1-SnTox1 and Tsn1-SnToxA interactions explained 22 and 28% of the variation in disease, respectively, and together they explained 48% indicating that their effects are largely additive. The Snn1-SnTox1 interaction accounted for 50% of the variation when the population was inoculated with an S. nodorum strain where the SnToxA gene had been mutated, eliminating the Tsn1-SnToxA interaction. These results support the theory that the wheat-S. nodorum pathosystem is largely based on multiple host-toxin interactions that follow an inverse gene-for-gene scenario at the host-toxin interface, but disease exhibits quantitative variation due to the mainly additive nature of compatible interactions. The elimination of either Snn1 or Tsn1 toxin sensitivity alleles resulted in decreased susceptibility, but the elimination of both interactions was required to obtain high levels of resistance. We propose the use of molecular markers to select against Snn1, Tsn1, and other toxin sensitivity alleles to develop wheat varieties with high levels of SNB resistance.

Indexed as

AscomycotaChromosome MappingDisease SusceptibilityGenes, PlantHaploidyHost-Pathogen InteractionsMycotoxinsPlant DiseasesQuantitative Trait LociSpores, FungalTriticumMycotoxins

Identifiers

PMID20084492
OpenAlexW1995815519

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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.