Evidence map›Paper›PMID 19023586›Full record

ReviewChromosoma2009

RNA turnover and chromatin-dependent gene silencing.

Marc Bühler

Abstract readReview
PubMed Publisher
In one paragraph

Review in Chromosoma, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Architectural RNA in chromatin organization.Biochemical Society transactions · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. mRNA quality control goes transcriptional.Biochemical Society transactions · 2013
    Review
  13. Chromatin-associated ncRNA activities.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2013
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

1 author at 1 institution in 1 country.

Marc BühlerFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland. marc.buehler@fmi.ch
Friedrich Miescher Institute · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the last few years, there has been a convergence of two seemingly disparate fields of study: chromatin-dependent gene silencing and RNA turnover. In contrast to RNA turnover mechanisms that operate on a truly posttranscriptional level, we are at the beginning of studies leading the way toward a model in which RNA turnover mechanisms are also involved in chromatin-dependent gene regulation. In particular, data from a variety of organisms have shown that the assembly of silent chromatin coincides with the presence or absence of non-protein-coding RNAs (ncRNAs). These range from long ncRNAs that have been classically implicated in the regulation of dosage compensation and genomic imprinting to small ncRNAs which are involved in heterochromatin assembly via the RNA interference (RNAi) pathway. This raises the question of how common ncRNAs are used to control gene expression at the level of chromatin. It is known at least, that they are present, as recent findings indicate that transcription of eukaryotic genomes is much more widespread than previously anticipated. However, the existence of a ncRNA does not prove its biological significance. Thus, a future challenge will be to distinguish the ncRNAs that are in some way meaningful to the organism from those that arise from the imperfect fidelity of the transcription machinery. Finally, no matter whether functional or not, RNAs transcribed from supposedly silent chromatin seem to be processed rapidly. Recent data from both fission and budding yeast suggest that chromatin-dependent gene silencing is achieved, at least in part, through RNA turnover mechanisms that use components of the RNAi pathway as well as polyadenylation-dependent RNA decay. Hence, silent chromatin is not only controlled transcriptionally, but also on co- and posttranscriptional levels.

Indexed as

Gene SilencingAnimalsCell CycleChromatinChromatin Assembly and DisassemblyEpigenesis, GeneticGene Expression ProfilingHeterochromatinHumansModels, GeneticRNARNA InterferenceChromatinHeterochromatinRNA

Identifiers

PMID19023586
OpenAlexW2089661916

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.