Evidence map›Paper›PMID 17524140›Full record

ArticleBMC genomics2007

Diverse histone modifications on histone 3 lysine 9 and their relation to DNA methylation in specifying gene silencing.

Jiejun Wu, Shu-Huei Wang, Dustin Potter, Joseph C Liu, Laura T Smith, Yue-Zhong Wu, Tim H-M Huang, Christoph Plass

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 44 citations in OpenAlex.

  1. Caloric restriction induced epigenetic effects on aging.Frontiers in cell and developmental biology · 2022
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  14. Mammalian DNA methyltransferases: a structural perspective.Structure (London, England : 1993) · 2008
    Review
  15. 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

8 authors at 2 institutions in 1 country.

Jiejun WuDepartment of Molecular Genetics, The Ohio State University, Columbus, OH, USA. Jiejun.Wu@osumc.edu <Jiejun.Wu@osumc.edu>
Shu-Huei Wang
Dustin Potter
Joseph C Liu
Laura T Smith
Yue-Zhong Wu
Tim H-M Huang
Christoph Plass
The Ohio State University · USCancer Genetics (United States) · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
Predicting Drug Resistance in Cancer Genomes by DMA Methylation ProfilingU54CA113001 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HUANG, TIM H.-M. · 2004 to 2014
$16.1M
PathologyP01CA101956 · NCI · OHIO STATE UNIVERSITY · PI BYRD, JOHN C. · 2006 to 2010
$11.4M
Postdoctoral Training in Cancer GeneticsT32CA106196 · NCI · OHIO STATE UNIVERSITY · PI DE LA CHAPELLE, ALBERT · 2004 to 2013
$3.6M
NCI NIH HHS N01 CO012400NCI NIH HHS N01-CO-12400NCI NIH HHS P01 CA101956NCI NIH HHS P01-CA101956-01NCI NIH HHS P30 CA016058NCI NIH HHS P30 CA16058NCI NIH HHS T32 CA106196NCI NIH HHS U54 CA113001
6 · The paper itself

Abstract

backgroundPrevious studies of individual genes have shown that in a self-enforcing way, dimethylation at histone 3 lysine 9 (dimethyl-H3K9) and DNA methylation cooperate to maintain a repressive mode of inactive genes. Less clear is whether this cooperation is generalized in mammalian genomes, such as mouse genome. Here we use epigenomic tools to simultaneously interrogate chromatin modifications and DNA methylation in a mouse leukemia cell line, L1210.

resultsHistone modifications on H3K9 and DNA methylation in L1210 were profiled by both global CpG island array and custom mouse promoter array analysis. We used chromatin immunoprecipitation microarray (ChIP-chip) to examine acetyl-H3K9 and dimethyl-H3K9. We found that the relative level of acetyl-H3K9 at different chromatin positions has a wider range of distribution than that of dimethyl-H3K9. We then used differential methylation hybridization (DMH) and the restriction landmark genome scanning (RLGS) to analyze the DNA methylation status of the same targets investigated by ChIP-chip. The results of epigenomic profiling, which have been independently confirmed for individual loci, show an inverse relationship between DNA methylation and histone acetylation in regulating gene silencing. In contrast to the previous notion, dimethyl-H3K9 seems to be less distinct in specifying silencing for the genes tested.

conclusionThis study demonstrates in L1210 leukemia cells a diverse relationship between histone modifications and DNA methylation in the maintenance of gene silencing. Acetyl-H3K9 shows an inverse relationship between DNA methylation and histone acetylation in regulating gene silencing as expected. However, dimethyl-H3K9 seems to be less distinct in relation to promoter methylation. Meanwhile, a combination of epigenomic tools is of help in understanding the heterogeneity of epigenetic regulation, which may further our vision accumulated from single-gene studies.

Indexed as

DNA MethylationGene SilencingProtein Processing, Post-TranslationalAcetylationAnimalsAzacitidineCell Line, TumorChromatin ImmunoprecipitationCpG IslandsDecitabineDNA Modification MethylasesGene Expression RegulationHistonesHydroxamic AcidsLeukemia L1210LysineAzacitidineDecitabineDNA Modification MethylasesHistonesHydroxamic AcidsLysinetrichostatin A

Identifiers

PMID17524140
PMCPMC1888705
OpenAlexW2012864657

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.