Evidence map›Paper›PMID 34990464›Full record

ArticlePLoS pathogens2022

Variability in an effector gene promoter of a necrotrophic fungal pathogen dictates epistasis and effector-triggered susceptibility in wheat.

Evan John, Silke Jacques, Huyen T T Phan, Lifang Liu, Danilo Pereira, Daniel Croll, Karam B Singh, Richard P Oliver, Kar-Chun Tan

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.2field-weighted citation impact, top 7% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Characterization and Genome Analysis ofJournal of fungi (Basel, Switzerland) · 2025
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  3. Review
  4. Article
  5. Article
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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

9 authors at 4 institutions in 2 countries.

Evan JohnCentre for Crop and Disease Management, Curtin University, Bentley, Perth, Western Australia, Australia.ORCID 0000-0002-7530-9665
Silke JacquesCentre for Crop and Disease Management, Curtin University, Bentley, Perth, Western Australia, Australia.ORCID 0000-0002-5464-4528
Huyen T T PhanCentre for Crop and Disease Management, Curtin University, Bentley, Perth, Western Australia, Australia.ORCID 0000-0002-8971-2308
Lifang LiuCentre for Crop and Disease Management, Curtin University, Bentley, Perth, Western Australia, Australia.
Danilo PereiraPlant Pathology, Institute of Integrative Biology, ETH Zurich, Zurich, Switzerland.ORCID 0000-0003-1247-242X
Daniel CrollLaboratory of Evolutionary Genetics, Institute of Biology, University of Neuchâtel, Neuchâtel, Switzerland.ORCID 0000-0002-2072-380X
Karam B SinghCentre for Crop and Disease Management, Curtin University, Bentley, Perth, Western Australia, Australia.ORCID 0000-0002-2777-7448
Richard P OliverCurtin University, Bentley, Perth, Western Australia, Australia.ORCID 0000-0001-7290-4154
Kar-Chun TanCentre for Crop and Disease Management, Curtin University, Bentley, Perth, Western Australia, Australia.ORCID 0000-0001-6094-823X
Curtin University · AUCommonwealth Scientific and Industrial Research Organisation · AUETH Zurich · CHUniversity of Neuchâtel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The fungus Parastagonospora nodorum uses proteinaceous necrotrophic effectors (NEs) to induce tissue necrosis on wheat leaves during infection, leading to the symptoms of septoria nodorum blotch (SNB). The NEs Tox1 and Tox3 induce necrosis on wheat possessing the dominant susceptibility genes Snn1 and Snn3B1/Snn3D1, respectively. We previously observed that Tox1 is epistatic to the expression of Tox3 and a quantitative trait locus (QTL) on chromosome 2A that contributes to SNB resistance/susceptibility. The expression of Tox1 is significantly higher in the Australian strain SN15 compared to the American strain SN4. Inspection of the Tox1 promoter region revealed a 401 bp promoter genetic element in SN4 positioned 267 bp upstream of the start codon that is absent in SN15, called PE401. Analysis of the world-wide P. nodorum population revealed that a high proportion of Northern Hemisphere isolates possess PE401 whereas the opposite was observed in representative P. nodorum isolates from Australia and South Africa. The presence of PE401 removed the epistatic effect of Tox1 on the contribution of the SNB 2A QTL but not Tox3. PE401 was introduced into the Tox1 promoter regulatory region in SN15 to test for direct regulatory roles. Tox1 expression was markedly reduced in the presence of PE401. This suggests a repressor molecule(s) binds PE401 and inhibits Tox1 transcription. Infection assays also demonstrated that P. nodorum which lacks PE401 is more pathogenic on Snn1 wheat varieties than P. nodorum carrying PE401. An infection competition assay between P. nodorum isogenic strains with and without PE401 indicated that the higher Tox1-expressing strain rescued the reduced virulence of the lower Tox1-expressing strain on Snn1 wheat. Our study demonstrated that Tox1 exhibits both 'selfish' and 'altruistic' characteristics. This offers an insight into a complex NE-NE interaction that is occurring within the P. nodorum population. The importance of PE401 in breeding for SNB resistance in wheat is discussed.

Indexed as

AscomycotaDisease ResistanceDisease SusceptibilityEpistasis, GeneticHost-Pathogen InteractionsMycosesPlant DiseasesPromoter Regions, GeneticQuantitative Trait LociTriticumVirulence

Identifiers

PMID34990464
PMCPMC8735624
OpenAlexW4225794010

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.