Evidence map›Paper›PMID 22570599›Full record

ArticlePLoS computational biology2012

Microarray analysis of LTR retrotransposon silencing identifies Hdac1 as a regulator of retrotransposon expression in mouse embryonic stem cells.

Judith Reichmann, James H Crichton, Monika J Madej, Mary Taggart, Philippe Gautier, Jose Luis Garcia-Perez, Richard R Meehan, Ian R Adams

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
11.3field-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

47 citing papers in PubMed, 72 citations in OpenAlex.

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  13. Methylation-directed glycosylation of chromatin factors represses retrotransposon promoters.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

8 authors at 4 institutions in 2 countries.

Judith ReichmannMRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom.
James H Crichton
Monika J Madej
Mary Taggart
Philippe Gautier
Jose Luis Garcia-Perez
Richard R Meehan
Ian R Adams
MRC Institute of Genetics and Molecular Medicine · GBWestern General Hospital · GBPfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research · ESUniversity of Edinburgh · GB

Funding

Medical Research Council MC_PC_U127574433Medical Research Council MC_PC_U127580973Medical Research Council MC_U127574433Medical Research Council MC_U127580973
6 · The paper itself

Abstract

Retrotransposons are highly prevalent in mammalian genomes due to their ability to amplify in pluripotent cells or developing germ cells. Host mechanisms that silence retrotransposons in germ cells and pluripotent cells are important for limiting the accumulation of the repetitive elements in the genome during evolution. However, although silencing of selected individual retrotransposons can be relatively well-studied, many mammalian retrotransposons are seldom analysed and their silencing in germ cells, pluripotent cells or somatic cells remains poorly understood. Here we show, and experimentally verify, that cryptic repetitive element probes present in Illumina and Affymetrix gene expression microarray platforms can accurately and sensitively monitor repetitive element expression data. This computational approach to genome-wide retrotransposon expression has allowed us to identify the histone deacetylase Hdac1 as a component of the retrotransposon silencing machinery in mouse embryonic stem cells, and to determine the retrotransposon targets of Hdac1 in these cells. We also identify retrotransposons that are targets of other retrotransposon silencing mechanisms such as DNA methylation, Eset-mediated histone modification, and Ring1B/Eed-containing polycomb repressive complexes in mouse embryonic stem cells. Furthermore, our computational analysis of retrotransposon silencing suggests that multiple silencing mechanisms are independently targeted to retrotransposons in embryonic stem cells, that different genomic copies of the same retrotransposon can be differentially sensitive to these silencing mechanisms, and helps define retrotransposon sequence elements that are targeted by silencing machineries. Thus repeat annotation of gene expression microarray data suggests that a complex interplay between silencing mechanisms represses retrotransposon loci in germ cells and embryonic stem cells.

Indexed as

AnimalsCells, CulturedEmbryonic Stem CellsGene Expression ProfilingGene Expression Regulation, DevelopmentalGene SilencingHistone Deacetylase 1Interspersed Repetitive SequencesMiceOligonucleotide Array Sequence AnalysisRegulatory Sequences, Nucleic AcidRetroelementsHdac1 protein, mouseHistone Deacetylase 1Retroelements

Identifiers

PMID22570599
PMCPMC3343110
OpenAlexW2052130036

What Socratic 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 Socratic graph.