Evidence map›Paper›PMID 23555272›Full record

ArticlePLoS pathogens2013

Pseudomonas syringae pv. syringae uses proteasome inhibitor syringolin A to colonize from wound infection sites.

Johana C Misas-Villamil, Izabella Kolodziejek, Emerson Crabill, Farnusch Kaschani, Sherry Niessen, Takayuki Shindo, Markus Kaiser, James R Alfano, Renier A L van der Hoorn

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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
12.0field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Characterization ofJournal of fungi (Basel, Switzerland) · 2024
    Article
  6. Review
  7. Article
  8. Plant susceptible responses: the underestimated side of plant-pathogen interactions.Biological reviews of the Cambridge Philosophical Society · 2022
    Review
  9. Review
  10. Review
  11. Article
  12. Inference of Convergent Gene Acquisition AmongFrontiers in microbiology · 2019
    Article
  13. Stomatal Defense a Decade Later.Plant physiology · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

9 authors at 4 institutions in 2 countries.

Johana C Misas-VillamilPlant Chemetics Lab, Max Planck Institute for Plant Breeding Research, Cologne, Germany.
Izabella Kolodziejek
Emerson Crabill
Farnusch Kaschani
Sherry Niessen
Takayuki Shindo
Markus Kaiser
James R Alfano
Renier A L van der Hoorn
Max Planck Institute for Plant Breeding Research · DEUniversity of Duisburg-Essen · DEUniversity of Nebraska–Lincoln · USScripps Research Institute · US

Funding

Suppression of innate immunity by an ADP-ribosyltransferase type III effectorR01AI069146 · NIAID · UNIVERSITY OF NEBRASKA LINCOLN · PI ALFANO, JAMES ROBERT · 2008 to 2012
$1.8M
NIAID NIH HHS 1R01AI069146-01A2NIAID NIH HHS R01 AI069146
6 · The paper itself

Abstract

Infection of plants by bacterial leaf pathogens at wound sites is common in nature. Plants defend wound sites to prevent pathogen invasion, but several pathogens can overcome spatial restriction and enter leaf tissues. The molecular mechanisms used by pathogens to suppress containment at wound infection sites are poorly understood. Here, we studied Pseudomonas syringae strains causing brown spot on bean and blossom blight on pear. These strains exist as epiphytes that can cause disease upon wounding caused by hail, sand storms and frost. We demonstrate that these strains overcome spatial restriction at wound sites by producing syringolin A (SylA), a small molecule proteasome inhibitor. Consequently, SylA-producing strains are able to escape from primary infection sites and colonize adjacent tissues along the vasculature. We found that SylA diffuses from the primary infection site and suppresses acquired resistance in adjacent tissues by blocking signaling by the stress hormone salicylic acid (SA). Thus, SylA diffusion creates a zone of SA-insensitive tissue that is prepared for subsequent colonization. In addition, SylA promotes bacterial motility and suppresses immune responses at the primary infection site. These local immune responses do not affect bacterial growth and were weak compared to effector-triggered immunity. Thus, SylA facilitates colonization from wounding sites by increasing bacterial motility and suppressing SA signaling in adjacent tissues.

Indexed as

Amino Acid SequenceHost-Pathogen InteractionsMolecular Sequence DataNicotianaPeptides, CyclicPlant DiseasesPlant ProteinsProteasome Endopeptidase ComplexProteasome InhibitorsPseudomonas syringaeSignal TransductionWound InfectionPeptides, CyclicPlant ProteinsProteasome Endopeptidase ComplexProteasome Inhibitorssyringolin A

Identifiers

PMID23555272
PMCPMC3610659
OpenAlexW2019512189

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.