Evidence map›Paper›PMID 16227595›Full record

ArticleMolecular and cellular biology2005

Dimethylation of histone H3 at lysine 36 demarcates regulatory and nonregulatory chromatin genome-wide.

Bhargavi Rao, Yoichiro Shibata, Brian D Strahl, Jason D Lieb

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 177 citations in OpenAlex.

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  13. Depletion of H3K36me2 recapitulates epigenomic and phenotypic changes induced by the H3.3K36M oncohistone mutation.Proceedings of the National Academy of Sciences of the United States of America · 2021
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44 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

4 authors at 2 institutions in 2 countries.

Bhargavi RaoDepartment of Biology, CB no. 3280, 203 Fordham Hall, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Yoichiro Shibata
Brian D Strahl
Jason D Lieb
Institut thématique Génétique, génomique et bioinformatique · FRUniversity of North Carolina at Chapel Hill · US

Funding

Role of Set2 and H3 methylation in chromatin functionR01GM068088 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI STRAHL, BRIAN D · 2003 to 2017
$3.4M
Understanding Specificity in Protein-Genome InteractionsK22HG002577 · NHGRI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI LIEB, JASON D · 2002 to 2004
$805k
NHGRI NIH HHS K22 HG 002577NHGRI NIH HHS K22 HG002577NIGMS NIH HHS R01 GM068088NIGMS NIH HHS R01 GM 68088
6 · The paper itself

Abstract

Set2p, which mediates histone H3 lysine 36 dimethylation (H3K36me2) in Saccharomyces cerevisiae, has been shown to associate with RNA polymerase II (RNAP II) at individual loci. Here, chromatin immunoprecipitation-microarray experiments normalized to general nucleosome occupancy reveal that nucleosomes within open reading frames (ORFs) and downstream noncoding chromatin were highly dimethylated at H3K36 and that Set2p activity begins at a stereotypic distance from the initiation of transcription genome-wide. H3K36me2 is scarce in regions upstream of divergently transcribed genes, telomeres, silenced mating loci, and regions transcribed by RNA polymerase III, providing evidence that the enzymatic activity of Set2p is restricted to its association with RNAP II. The presence of H3K36me2 within ORFs correlated with the "on" or "off" state of transcription, but the degree of H3K36 dimethylation within ORFs did not correlate with transcription frequency. This provides evidence that H3K36me2 is established during the initial instances of gene transcription, with subsequent transcription having at most a maintenance role. Accordingly, newly activated genes acquire H3K36me2 in a manner that does not correlate with gene transcript levels. Finally, nucleosomes dimethylated at H3K36 appear to be refractory to loss from highly transcribed chromatin. Thus, H3K36me2, which is highly conserved throughout eukaryotic evolution, provides a stable molecular mechanism for establishing chromatin context throughout the genome by distinguishing potential regulatory regions from transcribed chromatin.

Indexed as

Genome, FungalChromatinChromatin ImmunoprecipitationDNA PrimersHistonesLysineMethylationMethyltransferasesNucleosomesOpen Reading FramesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsChromatinDNA PrimersHistonesLysineMethyltransferasesNucleosomesSaccharomyces cerevisiae ProteinsSet2 protein, S cerevisiae

Identifiers

PMID16227595
PMCPMC1265832
OpenAlexW2135079976

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.