Evidence map›Paper›PMID 23431184›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

BIK1 interacts with PEPRs to mediate ethylene-induced immunity.

Zixu Liu, Ying Wu, Fan Yang, Yiyue Zhang, She Chen, Qi Xie, Xingjun Tian, Jian-Min Zhou

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed, 1 pooled it
42.5field-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

159 citing papers in PubMed, 1 synthesis or guideline pooled it, 331 citations in OpenAlex.

  1. Root colonization by beneficial rhizobacteria.FEMS microbiology reviews · 2024
    Pooled it
  2. Review
  3. Mechanisms and balanced regulation of plant immunity.Nature reviews. Molecular cell biology · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. PEPR1 Mediates SsNLP1-Triggered Immunity AgainstInternational journal of molecular sciences · 2026
    Article
  9. Review
  10. Article
  11. Review
  12. Plant cell surface receptors.The Plant journal : for cell and molecular biology · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

99 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 1 country.

Zixu LiuSchool of Life Science, Nanjing University, Nanjing 210093, China.
Ying Wu
Fan Yang
Yiyue Zhang
She Chen
Qi Xie
Xingjun Tian
Jian-Min Zhou
Chinese Academy of Sciences · CNNational Institute of Biological Sciences, Beijing · CNInstitute of Genetics and Developmental Biology · CNNanjing University · CNState Key Laboratory of Plant Genomics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plants have evolved intricate immune mechanisms to combat pathogen infection. Upon perception of pathogen-derived signals, plants accumulate defense hormones such as ethylene (ET), jasmonate, salicylate, and damage-associated molecular patterns to amplify immune responses. In particular, the Arabidopsis peptide Pep1 and its family members are thought to be damage-associated molecular patterns that trigger immunity through Pep1 receptor kinases PEPR1 and PEPR2. Here we show that PEPR1 specifically interacts with receptor-like cytoplasmic kinases botrytis-induced kinase 1 (BIK1) and PBS1-like 1 (PBL1) to mediate Pep1-induced defenses. In vitro and in vivo studies suggested that PEPR1, and likely PEPR2, directly phosphorylates BIK1 in response to Pep1 treatment. Surprisingly, the pepr1/pepr2 double-mutant seedlings displayed reduced in sensitivity to ET, as indicated by the elongated hypocotyls. ET-induced expression of defense genes and resistance to Botrytis cinerea were compromised in pepr1/pepr2 and bik1 mutants, reenforcing an important role of PEPRs and BIK1 in ET-mediated defense signaling. Pep treatment partially mimicked ET-induced seedling growth inhibition in a PEPR- and BIK1-dependent manner. Furthermore, both ET and Pep1 treatments induced BIK1 phosphorylation in a PEPR-dependent manner. However, the Pep1-induced BIK1 phosphorylation, seedling growth inhibition, and defense gene expression were independent of canonical ET signaling components. Together our results illustrate a mechanism by which ET and PEPR signaling pathways act in concert to amplify immune responses.

Indexed as

Plant ImmunityArabidopsisArabidopsis ProteinsDisease ResistanceDNA, ComplementaryEthylenesGenes, ReporterMutationPhosphorylationPlant Growth RegulatorsProtein Interaction Domains and MotifsProtein Serine-Threonine KinasesReceptors, Cell SurfaceRespiratory BurstSignal TransductionTwo-Hybrid System TechniquesArabidopsis ProteinsBIK1 protein, ArabidopsisDNA, ComplementaryethyleneEthylenesPEPR1 protein, ArabidopsisPEPR2 protein, ArabidopsisPlant Growth RegulatorsProtein Serine-Threonine KinasesReceptors, Cell Surface

Identifiers

PMID23431184
PMCPMC3625333
OpenAlexW1989636200

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.