Evidence map›Paper›PMID 29052528›Full record

ArticleBMC plant biology2017

Different genetic architectures underlie crop responses to the same pathogen: the {Helianthus annuus * Phoma macdonaldii} interaction case for black stem disease and premature ripening.

Amandine Bordat, Gwenaëlle Marchand, Nicolas B Langlade, Nicolas Pouilly, Stéphane Muños, Grégory Dechamp-Guillaume, Patrick Vincourt, Emmanuelle Bret-Mestries

Open access · goldAbstract read
In one paragraph

Article in BMC plant biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

2 citing papers in PubMed, 14 citations in OpenAlex.

  1. 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

8 authors at 4 institutions in 1 country.

Amandine BordatLIPM, Université de Toulouse, INRA, CNRS, Castanet-Tolosan, France.
Gwenaëlle MarchandLIPM, Université de Toulouse, INRA, CNRS, Castanet-Tolosan, France.
Nicolas B LangladeLIPM, Université de Toulouse, INRA, CNRS, Castanet-Tolosan, France.
Nicolas PouillyLIPM, Université de Toulouse, INRA, CNRS, Castanet-Tolosan, France.
Stéphane MuñosLIPM, Université de Toulouse, INRA, CNRS, Castanet-Tolosan, France.
Grégory Dechamp-GuillaumeENSAT, UMR 1248 AGIR, BP52627, F-31326, Castanet-Tolosan, France.
Patrick VincourtLIPM, Université de Toulouse, INRA, CNRS, Castanet-Tolosan, France.
Emmanuelle Bret-MestriesTerres Inovia, UMR 1248 AGIR, BP52627, F-31326, Castanet-Tolosan, France. e.mestries@terresinovia.fr.ORCID http://orcid.org/0000-0001-9876-5367
Centre National de la Recherche Scientifique · FRAGroecologies, Innovations & Ruralities · FRSaint-Gobain (France) · FRUniversité Fédérale de Toulouse Midi-Pyrénées · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPhoma macdonaldii has been reported as the causal agent of black stem disease (BS) and premature ripening (PR) on sunflower. PR is considered as the most widespread and detrimental disease on sunflower in France. While genetic variability and QTL mapping for partial resistance of sunflower to stem, collar and roots attacks have been reported on plantlets in controlled conditions, this work aims to describe the genetic variability in a subset of a sunflower lines, and for the first time to map QTL involved in PR resistance evaluated in field conditions using controlled inoculation.

resultsAn efficient and reliable method for inoculation used in field experiments induced stem base necrosis on up to 98% of all plants. A significant genetic variability for PR resistance in the field was detected among the 20 inbred lines of the core collection tested across the two years. For QTL mapping, the PR resistance evaluation was performed on two recombinant inbred lines (RIL) populations derived from the crosses XRQxPSC8 and FUxPAZ2 in two different years. QTL analyses were based on a newly developed consensus genetic map comprising 1007 non-redundant molecular markers. In each of the two RIL populations, different QTL involved in PR partial sunflower resistance were detected. The most significant QTL were detected 49 days post infection (DPI) on LG10 (LOD 7.7) and on LG7 (LOD 12.1) in the XRQxPSC8 and FUxPAZ2 RIL population, respectively. In addition, different QTL were detected on both populations for PR resistance measured between 14 and 35 DPI. In parallel, the incidence of natural attack of P. macdonaldii resulting in BS disease was recorded, showing that in these populations, the genetic of resistance to both diseases is not governed by the same factors.

conclusionThis work provides the first insights on the genetic architecture of sunflower PR resistance in the field. Moreover, the separate studies of symptoms on different organs and in time series allowed the identification of a succession of genetic components involved in the sunflower resistance to PR and BS diseases caused by Phoma macdonaldii along the development of the {plant * pathogen} interaction.

Indexed as

AscomycotaDisease ResistanceHelianthusHost-Pathogen InteractionsPlant DiseasesPlant RootsPlant StemsQuantitative Trait LociBlack stemPhoma macdonaldiiPremature ripeningQTL mappingSunflower

Identifiers

PMID29052528
PMCPMC5649070
OpenAlexW2767018829

What OpenQuestion holds

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LicenceCC BY
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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.