Evidence map›Paper›PMID 27217573›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Auxin-dependent compositional change in Mediator in ARF7- and ARF19-mediated transcription.

Jun Ito, Hidehiro Fukaki, Makoto Onoda, Lin Li, Chuanyou Li, Masao Tasaka, Masahiko Furutani

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
23.3field-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

50 citing papers in PubMed, 114 citations in OpenAlex.

  1. When MED16 Meets Plant Growth, Development, and Stress Response.International journal of molecular sciences · 2026
    Review
  2. Mechanisms of auxin action in plant growth and development.Nature reviews. Molecular cell biology · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. NLRs derepress MED10b- and MED7-mediated repression of jasmonate-dependent transcription to activate immunity.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. Article
  15. Article
  16. Do Opposites Attract? Auxin-Abscisic Acid Crosstalk: New Perspectives.International journal of molecular sciences · 2023
    Review
  17. RhizogenicProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. WOX11: the founder of plant organ regeneration.Cell regeneration (London, England) · 2023
    Review
  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

7 authors at 4 institutions in 2 countries.

Jun ItoGraduate School of Biological Sciences, Nara Institute of Science and Technology, Nara 630-0192, Japan;
Hidehiro FukakiDepartment of Biology, Graduate School of Science, Kobe University, Kobe 657-8501, Japan;
Makoto OnodaGraduate School of Biological Sciences, Nara Institute of Science and Technology, Nara 630-0192, Japan;
Lin LiInstitute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
Chuanyou LiInstitute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
Masao TasakaGraduate School of Biological Sciences, Nara Institute of Science and Technology, Nara 630-0192, Japan;
Masahiko FurutaniGraduate School of Biological Sciences, Nara Institute of Science and Technology, Nara 630-0192, Japan; ma-furut@agr.nagoya-u.ac.jp.
Nara Institute of Science and Technology · JPInstitute of Genetics and Developmental Biology · CNChinese Academy of Sciences · CNKobe University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mediator is a multiprotein complex that integrates the signals from transcription factors binding to the promoter and transmits them to achieve gene transcription. The subunits of Mediator complex reside in four modules: the head, middle, tail, and dissociable CDK8 kinase module (CKM). The head, middle, and tail modules form the core Mediator complex, and the association of CKM can modify the function of Mediator in transcription. Here, we show genetic and biochemical evidence that CKM-associated Mediator transmits auxin-dependent transcriptional repression in lateral root (LR) formation. The AUXIN/INDOLE 3-ACETIC ACID 14 (Aux/IAA14) transcriptional repressor inhibits the transcriptional activity of its binding partners AUXIN RESPONSE FACTOR 7 (ARF7) and ARF19 by making a complex with the CKM-associated Mediator. In addition, TOPLESS (TPL), a transcriptional corepressor, forms a bridge between IAA14 and the CKM component MED13 through the physical interaction. ChIP assays show that auxin induces the dissociation of MED13 but not the tail module component MED25 from the ARF7 binding region upstream of its target gene. These findings indicate that auxin-induced degradation of IAA14 changes the module composition of Mediator interacting with ARF7 and ARF19 in the upstream region of their target genes involved in LR formation. We suggest that this regulation leads to a quick switch of signal transmission from ARFs to target gene expression in response to auxin.

Indexed as

ArabidopsisArabidopsis ProteinsGene Expression Regulation, PlantIndoleacetic AcidsPlants, Genetically ModifiedRepressor ProteinsTranscription FactorsTranscription, GeneticArabidopsis ProteinsARF19 protein, ArabidopsisARF7 protein, ArabidopsisGRAND CENTRAL protein, ArabidopsisIAA14 protein, ArabidopsisIndoleacetic AcidsRepressor ProteinsTranscription Factorsauxin responseCDK8 kinase modulelateral root formationMediator complex

Identifiers

PMID27217573
PMCPMC4988599
OpenAlexW2403925542

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.