Evidence map›Paper›PMID 15514067›Full record

ArticleGenetics2004

Epigenetic control of CACTA transposon mobility in Arabidopsis thaliana.

Masaomi Kato, Kazuya Takashima, Tetsuji Kakutani

Abstract read
In one paragraph

Article in Genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Silencing ofGenetics · 2020
    Article
  11. Review
  12. Review
  13. Article
  14. Targeted DNA demethylation of theProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Epiallelic variation in Arabidopsis thaliana.Cold Spring Harbor symposia on quantitative biology · 2012
    Review
  20. Review
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.

Masaomi KatoDepartment of Integrated Genetics, National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan.
Kazuya Takashima
Tetsuji Kakutani

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic mutation, heritable developmental variation not based on a change in nucleotide sequence, is widely reported in plants. However, the developmental and evolutionary significance of such mutations remains enigmatic. On the basis of our studies of the endogenous Arabidopsis transposon CACTA, we propose that the inheritance of epigenetic gene silencing over generations can function as a transgenerational genome defense mechanism against deleterious movement of transposons. We previously reported that silent CACTA1 is mobilized by the DNA hypomethylation mutation ddm1 (decrease in DNA methylation). In this study, we report that CACTA activated by the ddm1 mutation remains mobile in the presence of the wild-type DDM1 gene, suggesting that de novo silencing is not efficient for the defense of the genome against CACTA movement. The defense depends on maintenance of transposon silencing over generations. In addition, we show that the activated CACTA1 element transposes throughout the genome in DDM1 plants, as reported previously for ddm1 backgrounds. Furthermore, the CACTA1 element integrated into both the ddm1-derived and the DDM1-derived chromosomal regions in the DDM1 wild-type plants, demonstrating that this class of transposons does not exhibit targeted integration into heterochromatin, despite its accumulation in the pericentromeric regions in natural populations. The possible contribution of natural selection as a mechanism for the accumulation of transposons and evolution of heterochromatin is discussed.

Indexed as

DNA MethylationGenetic VariationGenome, PlantArabidopsisArabidopsis ProteinsDNA-Binding ProteinsDNA Transposable ElementsGene SilencingHeterochromatinMutationPromoter Regions, GeneticSelection, GeneticTranscription FactorsArabidopsis ProteinsDDM1 protein, ArabidopsisDNA-Binding ProteinsDNA Transposable ElementsHeterochromatinTranscription Factors

Identifiers

PMID15514067
PMCPMC1448851

What OpenQuestion holds

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Registered trials

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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.