Evidence map›Paper›PMID 30235212›Full record

ArticlePLoS genetics2018

Modulation of ACD6 dependent hyperimmunity by natural alleles of an Arabidopsis thaliana NLR resistance gene.

Wangsheng Zhu, Maricris Zaidem, Anna-Lena Van de Weyer, Rafal M Gutaker, Eunyoung Chae, Sang-Tae Kim, Felix Bemm, Lei Li, Marco Todesco, Rebecca Schwab and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
7.4field-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

14 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  11. Cell Death in Plant Immunity.Cold Spring Harbor perspectives in biology · 2020
    Review
  12. Article
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  14. 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

14 authors at 1 institution in 1 country.

Wangsheng ZhuDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.ORCID 0000-0001-7773-3438
Maricris ZaidemDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.
Anna-Lena Van de WeyerDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.ORCID 0000-0002-5180-897X
Rafal M GutakerResearch Group for Ancient Genomics and Evolution, Max Planck Institute for Developmental Biology, Tübingen, Germany.ORCID 0000-0001-9226-879X
Eunyoung ChaeDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.ORCID 0000-0002-0889-9837
Sang-Tae KimDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.
Felix BemmDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.ORCID 0000-0001-6557-4898
Lei LiDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.
Marco TodescoDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.
Rebecca SchwabDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.ORCID 0000-0001-9933-9669
Frederik UngerDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.
Marcel Janis BehaDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.
Monika DemarDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.
Detlef WeigelDepartment of Molecular Biology, Max Planck Institute for Developmental Biology, Tübingen, Germany.
Max Planck Institute for Developmental Biology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plants defend themselves against pathogens by activating an array of immune responses. Unfortunately, immunity programs may also cause unintended collateral damage to the plant itself. The quantitative disease resistance gene ACCELERATED CELL DEATH 6 (ACD6) serves to balance growth and pathogen resistance in natural populations of Arabidopsis thaliana. An autoimmune allele, ACD6-Est, which strongly reduces growth under specific laboratory conditions, is found in over 10% of wild strains. There is, however, extensive variation in the strength of the autoimmune phenotype expressed by strains with an ACD6-Est allele, indicative of genetic modifiers. Quantitative genetic analysis suggests that ACD6 activity can be modulated in diverse ways, with different strains often carrying different large-effect modifiers. One modifier is SUPPRESSOR OF NPR1-1, CONSTITUTIVE 1 (SNC1), located in a highly polymorphic cluster of nucleotide-binding domain and leucine-rich repeat (NLR) immune receptor genes, which are prototypes for qualitative disease resistance genes. Allelic variation at SNC1 correlates with ACD6-Est activity in multiple accessions, and a common structural variant affecting the NL linker sequence can explain differences in SNC1 activity. Taken together, we find that an NLR gene can mask the activity of an ACD6 autoimmune allele in natural A. thaliana populations, thereby linking different arms of the plant immune system.

Indexed as

AllelesAnkyrinsArabidopsisArabidopsis ProteinsAutoimmunityDisease ResistanceGene Expression Regulation, PlantMutationPlant DiseasesPlant ImmunityPlants, Genetically ModifiedSignal TransductionACD6 protein, ArabidopsisAnkyrinsArabidopsis ProteinsSNC1 protein, Arabidopsis

Identifiers

PMID30235212
PMCPMC6168153
OpenAlexW2949387242

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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.