Evidence map›Paper›PMID 26866607›Full record

ArticlePLoS genetics2016

The Quantitative Basis of the Arabidopsis Innate Immune System to Endemic Pathogens Depends on Pathogen Genetics.

Jason A Corwin, Daniel Copeland, Julie Feusier, Anushriya Subedy, Robert Eshbaugh, Christine Palmer, Julin Maloof, Daniel J Kliebenstein

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
26.0field-weighted citation impact, top 1% 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

45 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
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  3. Combined generalist and host-specific transcriptional strategies enable host generalism in the fungal pathogenProceedings of the National Academy of Sciences of the United States of America · 2026
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  5. A multiplant transcriptomic atlas reveals conserved and lineage-specific defense architectures in response toProceedings of the National Academy of Sciences of the United States of America · 2026
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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 2 institutions in 2 countries.

Jason A CorwinDepartment of Plant Sciences, College of Agricultural and Environmental Sciences, University of California - Davis, Davis, California, United States of America.
Daniel CopelandDepartment of Plant Sciences, College of Agricultural and Environmental Sciences, University of California - Davis, Davis, California, United States of America.
Julie FeusierDepartment of Plant Sciences, College of Agricultural and Environmental Sciences, University of California - Davis, Davis, California, United States of America.
Anushriya SubedyDepartment of Plant Sciences, College of Agricultural and Environmental Sciences, University of California - Davis, Davis, California, United States of America.
Robert EshbaughDepartment of Plant Sciences, College of Agricultural and Environmental Sciences, University of California - Davis, Davis, California, United States of America.
Christine PalmerDepartment of Plant Biology, College of Biological Sciences, University of California - Davis, Davis, California, United States of America.
Julin MaloofDepartment of Plant Biology, College of Biological Sciences, University of California - Davis, Davis, California, United States of America.
Daniel J KliebensteinDepartment of Plant Sciences, College of Agricultural and Environmental Sciences, University of California - Davis, Davis, California, United States of America.
University of California, Davis · USUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The most established model of the eukaryotic innate immune system is derived from examples of large effect monogenic quantitative resistance to pathogens. However, many host-pathogen interactions involve many genes of small to medium effect and exhibit quantitative resistance. We used the Arabidopsis-Botrytis pathosystem to explore the quantitative genetic architecture underlying host innate immune system in a population of Arabidopsis thaliana. By infecting a diverse panel of Arabidopsis accessions with four phenotypically and genotypically distinct isolates of the fungal necrotroph B. cinerea, we identified a total of 2,982 genes associated with quantitative resistance using lesion area and 3,354 genes associated with camalexin production as measures of the interaction. Most genes were associated with resistance to a specific Botrytis isolate, which demonstrates the influence of pathogen genetic variation in analyzing host quantitative resistance. While known resistance genes, such as receptor-like kinases (RLKs) and nucleotide-binding site leucine-rich repeat proteins (NLRs), were found to be enriched among associated genes, they only account for a small fraction of the total genes associated with quantitative resistance. Using publically available co-expression data, we condensed the quantitative resistance associated genes into co-expressed gene networks. GO analysis of these networks implicated several biological processes commonly connected to disease resistance, including defense hormone signaling and ROS production, as well as novel processes, such as leaf development. Validation of single gene T-DNA knockouts in a Col-0 background demonstrate a high success rate (60%) when accounting for differences in environmental and Botrytis genetic variation. This study shows that the genetic architecture underlying host innate immune system is extremely complex and is likely able to sense and respond to differential virulence among pathogen genotypes.

Indexed as

Immunity, InnateArabidopsisBotrytisChromosome MappingGene Expression Regulation, PlantGene OntologyGene Regulatory NetworksGenes, PlantGenome-Wide Association StudyGenotypeHost-Pathogen InteractionsIndolesLinear ModelsPhenotypePhytoalexinsReproducibility of ResultscamalexinIndolesPhytoalexinsThiazoles

Identifiers

PMID26866607
PMCPMC4750985
OpenAlexW2253018663

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.