Evidence map›Paper›PMID 29177423›Full record

ArticlePlant & cell physiology2018

Salicylic Acid and Jasmonic Acid Pathways are Activated in Spatially Different Domains Around the Infection Site During Effector-Triggered Immunity in Arabidopsis thaliana.

Shigeyuki Betsuyaku, Shinpei Katou, Yumiko Takebayashi, Hitoshi Sakakibara, Nobuhiko Nomura, Hiroo Fukuda

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Plant & cell physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 79 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 2 pooled it
32.9field-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

79 citing papers in PubMed, 2 syntheses or guidelines pooled it, 224 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Spatial organization of plant defense at the infection front.bioRxiv : the preprint server for biology · 2026
    Article
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  9. Strengths and Limitations of Salicylic Acid Reporters.International journal of molecular sciences · 2025
    Review
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19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Shigeyuki BetsuyakuFaculty of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibarakim 305-8577 Japan.
Shinpei KatouInstitute of Agriculture, Academic Assembly, Shinshu University, 8304, Minamiminowa, Nagano, 399-4598 Japan.
Yumiko TakebayashiPlant Productivity Systems Research Group, RIKEN Center for Sustainable Resource Science, 1-7-22, Suehiro, Tsurumi-ku, Yokohama, 230-0045 Japan.
Hitoshi SakakibaraPlant Productivity Systems Research Group, RIKEN Center for Sustainable Resource Science, 1-7-22, Suehiro, Tsurumi-ku, Yokohama, 230-0045 Japan.
Nobuhiko NomuraFaculty of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibarakim 305-8577 Japan.
Hiroo FukudaDepartment of Biological Sciences, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
RIKEN Center for Sustainable Resource Science · JPUniversity of Tsukuba · JPShinshu University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The innate immune response is, in the first place, elicited at the site of infection. Thus, the host response can be different among the infected cells and the cells surrounding them. Effector-triggered immunity (ETI), a form of innate immunity in plants, is triggered by specific recognition between pathogen effectors and their corresponding plant cytosolic immune receptors, resulting in rapid localized cell death known as hypersensitive response (HR). HR cell death is usually limited to a few cells at the infection site, and is surrounded by a few layers of cells massively expressing defense genes such as Pathogenesis-Related Gene 1 (PR1). This virtually concentric pattern of the cellular responses in ETI is proposed to be regulated by a concentration gradient of salicylic acid (SA), a phytohormone accumulated around the infection site. Recent studies demonstrated that jasmonic acid (JA), another phytohormone known to be mutually antagonistic to SA in many cases, is also accumulated in and required for ETI, suggesting that ETI is a unique case. However, the molecular basis for this uniqueness remained largely to be solved. Here, we found that, using intravital time-lapse imaging, the JA signaling pathway is activated in the cells surrounding the central SA-active cells around the infection sites in Arabidopsis thaliana. This distinct spatial organization explains how these two phythormone pathways in a mutually antagonistic relationship can be activated simultaneously during ETI. Our results re-emphasize that the spatial consideration is a key strategy to gain mechanistic insights into the apparently complex signaling cross-talk in immunity.

Indexed as

Signal TransductionArabidopsisArabidopsis ProteinsCyclopentanesHost-Pathogen InteractionsMicroscopy, ConfocalOxylipinsPlant DiseasesPlant ImmunityPlants, Genetically ModifiedPseudomonas syringaeSalicylic AcidTime-Lapse ImagingArabidopsis ProteinsCyclopentanesjasmonic acidOxylipinsPR-1 protein, ArabidopsisSalicylic AcidArabidopsis thalianaEffector-triggered immunityJasmonic acidPseudomonas syringae pv. tomato DC3000 carrying AvrRpt2Salicylic acidTime-lapse imaging

Identifiers

PMID29177423
PMCPMC6012717
OpenAlexW2768938249

What OpenQuestion holds

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LicenceCC BY-NC
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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.