Evidence map›Paper›PMID 23785289›Full record

ArticlePLoS pathogens2013

The Xanthomonas campestris type III effector XopJ targets the host cell proteasome to suppress salicylic-acid mediated plant defence.

Suayib Üstün, Verena Bartetzko, Frederik Börnke

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
19.4field-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

59 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Article
  6. Review
  7. Article
  8. Autophagy and Bacterial infections.Autophagy reports · 2025
    Review
  9. Article
  10. Article
  11. The Type III Effector XopLInternational journal of molecular sciences · 2024
    Article
  12. Article
  13. Functional Analysis of Type III Effectors inPathogens (Basel, Switzerland) · 2024
    Article
  14. A Pipeline to Monitor Proteasome Homeostasis in Plants.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  15. Article
  16. N-MethyltransferaseInternational journal of molecular sciences · 2022
    Article
  17. Article
  18. Review
  19. Review
  20. The Same against Many: AtCML8, a CaInternational journal of molecular sciences · 2021
    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

3 authors at 1 institution in 1 country.

Suayib ÜstünFriedrich-Alexander-University Erlangen-Nuremberg, Department of Biology, Division of Biochemistry, Erlangen, Germany.
Verena Bartetzko
Frederik Börnke
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The phytopathogenic bacterium Xanthomonas campestris pv. vesicatoria (Xcv) requires type III effector proteins (T3Es) for virulence. After translocation into the host cell, T3Es are thought to interact with components of host immunity to suppress defence responses. XopJ is a T3E protein from Xcv that interferes with plant immune responses; however, its host cellular target is unknown. Here we show that XopJ interacts with the proteasomal subunit RPT6 in yeast and in planta to inhibit proteasome activity. A C235A mutation within the catalytic triad of XopJ as well as a G2A exchange within the N-terminal myristoylation motif abolishes the ability of XopJ to inhibit the proteasome. Xcv ΔxopJ mutants are impaired in growth and display accelerated symptom development including tissue necrosis on susceptible pepper leaves. Application of the proteasome inhibitor MG132 restored the ability of the Xcv ΔxopJ to attenuate the development of leaf necrosis. The XopJ dependent delay of tissue degeneration correlates with reduced levels of salicylic acid (SA) and changes in defence- and senescence-associated gene expression. Necrosis upon infection with Xcv ΔxopJ was greatly reduced in pepper plants with reduced expression of NPR1, a central regulator of SA responses, demonstrating the involvement of SA-signalling in the development of XopJ dependent phenotypes. Our results suggest that XopJ-mediated inhibition of the proteasome interferes with SA-dependent defence response to attenuate onset of necrosis and to alter host transcription. A central role of the proteasome in plant defence is discussed.

Indexed as

Signal TransductionBacterial ProteinsCapsicumHost-Pathogen InteractionsMutationNicotianaPlant DiseasesPlant ProteinsProteasome Endopeptidase ComplexSalicylic AcidTranscription, GeneticXanthomonas campestrisBacterial ProteinsPlant ProteinsProteasome Endopeptidase ComplexSalicylic Acid

Identifiers

PMID23785289
PMCPMC3681735
OpenAlexW1971290111

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.