Evidence map›Paper›PMID 25881024›Full record

ArticleBMC genomics2015

Different distribution of histone modifications in genes with unidirectional and bidirectional transcription and a role of CTCF and cohesin in directing transcription.

Susanne Bornelöv, Jan Komorowski, Claes Wadelius

Abstract readComparative Study
In one paragraph

Article in BMC genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Molecular models of bidirectional promoter regulation.Current opinion in structural biology · 2024
    Review
  4. Article
  5. Article
  6. Article
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  8. Article
  9. Article
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  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. CTCF: making the right connections.Genes & development · 2016
    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.

Susanne BornelövDepartment of Cell and Molecular Biology, Science for Life Laboratory, Uppsala University, Uppsala, SE-751 24, Sweden. susanne.bornelov@imbim.uu.se.
Jan KomorowskiDepartment of Cell and Molecular Biology, Science for Life Laboratory, Uppsala University, Uppsala, SE-751 24, Sweden. jan.komorowski@icm.uu.se.
Claes WadeliusScience for Life Laboratory, Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, SE-751 08, Sweden. claes.wadelius@igp.uu.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral post-translational histone modifications are mainly found in gene promoters and are associated with the promoter activity. It has been hypothesized that histone modifications regulate the transcription, as opposed to the traditional view with transcription factors as the key regulators. Promoters of most active genes do not only initiate transcription of the coding sequence, but also a substantial amount of transcription of the antisense strand upstream of the transcription start site (TSS). This promoter feature has generally not been considered in previous studies of histone modifications and transcription factor binding.

resultsWe annotated protein-coding genes as bi- or unidirectional depending on their mode of transcription and compared histone modifications and transcription factor occurrences between them. We found that H3K4me3, H3K9ac, and H3K27ac were significantly more enriched upstream of the TSS in bidirectional genes compared with the unidirectional ones. In contrast, the downstream histone modification signals were similar, suggesting that the upstream histone modifications might be a consequence of transcription rather than a cause. Notably, we found well-positioned CTCF and RAD21 peaks approximately 60-80 bp upstream of the TSS in the unidirectional genes. The peak heights were related to the amount of antisense transcription and we hypothesized that CTCF and cohesin act as a barrier against antisense transcription.

conclusionsOur results provide insights into the distribution of histone modifications at promoters and suggest a novel role of CTCF and cohesin as regulators of transcriptional direction.

Indexed as

Transcription, GeneticCCCTC-Binding FactorCell Cycle ProteinsCell LineChromosomal Proteins, Non-HistoneCohesinsDNA-Binding ProteinsHep G2 CellsHistonesHumansHuman Umbilical Vein Endothelial CellsK562 CellsNuclear ProteinsPhosphoproteinsPromoter Regions, GeneticProtein Processing, Post-TranslationalCCCTC-Binding FactorCell Cycle ProteinsChromosomal Proteins, Non-HistoneCohesinsCTCF protein, humanDNA-Binding ProteinsHistonesNuclear ProteinsPhosphoproteinsRAD21 protein, humanRepressor Proteins

Identifiers

PMID25881024
PMCPMC4446127

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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.