Evidence map›Paper›PMID 22331359›Full record

ArticleJournal of cell science2012

Epigenetic engineering: histone H3K9 acetylation is compatible with kinetochore structure and function.

Jan H Bergmann, Julia N Jakubsche, Nuno M Martins, Alexander Kagansky, Megumi Nakano, Hiroshi Kimura, David A Kelly, Bryan M Turner, Hiroshi Masumoto, Vladimir Larionov and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing 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

76 citing papers in PubMed, 114 citations in OpenAlex.

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  15. Ccp1-Ndc80 switch at the N terminus of CENP-T regulates kinetochore assembly.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  16. Review
  17. Kinetochore assembly throughout the cell cycle.Seminars in cell & developmental biology · 2021
    Article
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  19. Article
  20. Article

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

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

11 authors at 6 institutions in 3 countries.

Jan H BergmannWellcome Trust Centre for Cell Biology, University of Edinburgh, King's Building, Mayfield Road, Edinburgh EH9 3JR, UK.
Julia N Jakubsche
Nuno M Martins
Alexander Kagansky
Megumi Nakano
Hiroshi Kimura
David A Kelly
Bryan M Turner
Hiroshi Masumoto
Vladimir Larionov
William C Earnshaw
University of Edinburgh · GBWellcome Centre for Cell Biology · GBKazusa DNA Research Institute · JPNational Institutes of Health · USOsaka University · JPUniversity of Birmingham · GB

Funding

Study of hereditary prostate cancer and human artificial chromosomesZIABC010413 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LARIONOV, VLADIMIR · 2009 to 2025
$31.5M
Intramural NIH HHSWellcome Trust 073915Wellcome Trust 080458Wellcome Trust 092076
6 · The paper itself

Abstract

Human kinetochores are transcriptionally active, producing very low levels of transcripts of the underlying alpha-satellite DNA. However, it is not known whether kinetochores can tolerate acetylated chromatin and the levels of transcription that are characteristic of housekeeping genes, or whether kinetochore-associated 'centrochromatin', despite being transcribed at a low level, is essentially a form of repressive chromatin. Here, we have engineered two types of acetylated chromatin within the centromere of a synthetic human artificial chromosome. Tethering a minimal NF-κB p65 activation domain within kinetochore-associated chromatin produced chromatin with high levels of histone H3 acetylated on lysine 9 (H3K9ac) and an ~10-fold elevation in transcript levels, but had no substantial effect on kinetochore assembly or function. By contrast, tethering the herpes virus VP16 activation domain produced similar modifications in the chromatin but resulted in an ~150-fold elevation in transcripts, approaching the level of transcription of an endogenous housekeeping gene. This rapidly inactivated kinetochores, causing a loss of assembled CENP-A and blocking further CENP-A assembly. Our data reveal that functional centromeres in vivo show a remarkable plasticity--kinetochores tolerate profound changes to their chromatin environment, but appear to be critically sensitive to the level of centromeric transcription.

Indexed as

Epigenesis, GeneticAcetylationAutoantigensCell LineCentromereCentromere Protein AChromatinChromosomal Proteins, Non-HistoneChromosomes, Artificial, HumanHerpes Simplex Virus Protein Vmw65HistonesHumansKinetochoresLysineRecombinant Fusion ProteinsTranscription Factor RelAAutoantigensCENPA protein, humanCentromere Protein AChromatinChromosomal Proteins, Non-HistoneHerpes Simplex Virus Protein Vmw65HistonesLysineRecombinant Fusion ProteinsTranscription Factor RelA

Identifiers

PMID22331359
PMCPMC3283876
OpenAlexW2145670790

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.