Evidence map›Paper›PMID 25831497›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

The frequency natural antisense transcript first promotes, then represses, frequency gene expression via facultative heterochromatin.

Na Li, Tammy M Joska, Catherine E Ruesch, Samuel J Coster, William J Belden

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Antisense Transcription of theJournal of biological rhythms · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
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  14. Review
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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

5 authors at 1 institution in 1 country.

Na LiDepartment of Animal Sciences, School of Environmental and Biological Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ 08901.
Tammy M JoskaDepartment of Animal Sciences, School of Environmental and Biological Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ 08901.
Catherine E RueschDepartment of Animal Sciences, School of Environmental and Biological Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ 08901.
Samuel J CosterDepartment of Animal Sciences, School of Environmental and Biological Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ 08901.
William J BeldenDepartment of Animal Sciences, School of Environmental and Biological Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ 08901 belden@aesop.rutgers.edu.
Rutgers, The State University of New Jersey · US

Funding

Examining Circadian Changes in Genome StructureR01GM101378 · NIGMS · RUTGERS, THE STATE UNIV OF N.J. · PI BELDEN, WILLIAM J · 2012 to 2016
$1.5M
NIGMS NIH HHS R01 GM101378NIGMS NIH HHS R01GM101378
6 · The paper itself

Abstract

The circadian clock is controlled by a network of interconnected feedback loops that require histone modifications and chromatin remodeling. Long noncoding natural antisense transcripts (NATs) originate from Period in mammals and frequency (frq) in Neurospora. To understand the role of NATs in the clock, we put the frq antisense transcript qrf (frq spelled backwards) under the control of an inducible promoter. Replacing the endogenous qrf promoter altered heterochromatin formation and DNA methylation at frq. In addition, constitutive, low-level induction of qrf caused a dramatic effect on the endogenous rhythm and elevated circadian output. Surprisingly, even though qrf is needed for heterochromatic silencing, induction of qrf initially promoted frq gene expression by creating a more permissible local chromatin environment. The observation that antisense expression can initially promote sense gene expression before silencing via heterochromatin formation at convergent loci is also found when a NAT to hygromycin resistance gene is driven off the endogenous vivid (vvd) promoter in the Δvvd strain. Facultative heterochromatin silencing at frq functions in a parallel pathway to previously characterized VVD-dependent silencing and is needed to establish the appropriate circadian phase. Thus, repression via dicer-independent siRNA-mediated facultative heterochromatin is largely independent of, and occurs alongside, other feedback processes.

Indexed as

Gene Expression RegulationBiological ClocksCircadian RhythmCLOCK ProteinsDNA MethylationGene Expression Regulation, FungalHeterochromatinHistonesNeurospora crassaOligonucleotides, AntisenseOscillometryPromoter Regions, GeneticRNA, Long NoncodingRNA, Small InterferingCLOCK ProteinsHeterochromatinHistonesOligonucleotides, AntisenseRNA, Long NoncodingRNA, Small Interferingcircadian rhythmDNA methylationheterochromatinnatural antisense transcripts

Identifiers

PMID25831497
PMCPMC4394252
OpenAlexW2085856891

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.