Evidence map›Paper›PMID 17431038›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Plastidial fatty acid levels regulate resistance gene-dependent defense signaling in Arabidopsis.

A C Chandra-Shekara, Srivathsa C Venugopal, Subhankar Roy Barman, Aardra Kachroo, Pradeep Kachroo

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. 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
13.3field-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, 97 citations in OpenAlex.

  1. Article
  2. Article
  3. Lipids and Lipid-Mediated Signaling in Plant-Pathogen Interactions.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. A Novel Glycerol Kinase GeneFrontiers in plant science · 2021
    Article
  10. Article
  11. Molecular plant-microbe interactions : MPMI · 2020
    Article
  12. Article
  13. Frontiers in microbiology · 2019
    Article
  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

5 authors at 1 institution in 1 country.

A C Chandra-ShekaraDepartment of Plant Pathology, University of Kentucky, Lexington, KY 40546, USA.
Srivathsa C Venugopal
Subhankar Roy Barman
Aardra Kachroo
Pradeep Kachroo
University of Kentucky · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In Arabidopsis, resistance to Turnip Crinkle Virus (TCV) depends on the resistance (R) gene, HRT, and the recessive locus rrt. Resistance also depends on salicylic acid (SA), EDS1, and PAD4. Exogenous application of SA confers resistance in RRT-containing plants by increasing HRT transcript levels in a PAD4-dependent manner. Here we report that reduction of oleic acid (18:1) can also induce HRT gene expression and confer resistance to TCV. However, the 18:1-regulated pathway is independent of SA, rrt, EDS1, and PAD4. Reducing the levels of 18:1, via a mutation in the SSI2-encoded stearoyl-acyl carrier protein-desaturase, or by exogenous application of glycerol, increased transcript levels of HRT as well as several other R genes. Second-site mutations in the ACT1-encoded glycerol-3-phosphate acyltransferase or GLY1-encoded glycerol-3-phosphate dehydrogenase restored 18:1 levels in HRT ssi2 plants and reestablished a dependence on rrt. Resistance to TCV and HRT gene expression in HRT act1 plants was inducible by SA but not by glycerol, whereas that in HRT pad4 plants was inducible by glycerol but not by SA. The low 18:1-mediated induction of R gene expression was also dependent on ACT1 but independent of EDS1, PAD4, and RAR1. Intriguingly, TCV inoculation did not activate this 18:1-regulated pathway in HRT plants, but instead resulted in the induction of several genes that encode 18:1-synthesizing isozymes. These results suggest that the 18:1-regulated pathway may be specifically targeted during pathogen infection and that altering 18:1 levels may serve as a unique strategy for promoting disease resistance.

Indexed as

Genes, PlantSignal TransductionArabidopsisArabidopsis ProteinsCarboxylic Ester HydrolasesCarmovirusDNA-Binding ProteinsEnzyme InductionFatty Acid DesaturasesGene Expression Regulation, PlantGlycerolGlycerol-3-Phosphate O-AcyltransferaseImmunity, InnateIsoenzymesMutationOleic AcidArabidopsis ProteinsCarboxylic Ester HydrolasesDNA-Binding ProteinsFatty Acid DesaturasesGlycerolGlycerol-3-Phosphate O-AcyltransferaseHRT protein, ArabidopsisIsoenzymesOleic AcidPAD4 protein, Arabidopsisplastidic glycerol-3-phosphate acyltransferase, ArabidopsisRepressor ProteinsRNA, MessengerSalicylic Acidstearoyl ACP desaturase, Arabidopsis

Identifiers

PMID17431038
PMCPMC1855359
OpenAlexW2059771885

What OpenQuestion holds

Textmetadata
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.