Evidence map›Paper›PMID 19022951›Full record

ArticleThe Journal of nutrition2008

Biotinylation of histones represses transposable elements in human and mouse cells and cell lines and in Drosophila melanogaster.

Yap Ching Chew, John T West, Stephanie J Kratzer, Anne M Ilvarsonn, Joel C Eissenberg, Bhavana J Dave, David Klinkebiel, Judith K Christman, Janos Zempleni

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of nutrition, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 75 citations in OpenAlex.

  1. Trial
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  4. Detection of metabolic adaptation in a triple-negative breast cancer animal model with [European journal of nuclear medicine and molecular imaging · 2024
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  9. Dietary Modulation of the Epigenome.Physiological reviews · 2018
    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

9 authors at 5 institutions in 1 country.

Yap Ching ChewDepartment of Nutrition and Health Sciences, University of Nebraska, Lincoln, NE 68583, USA.
John T West
Stephanie J Kratzer
Anne M Ilvarsonn
Joel C Eissenberg
Bhavana J Dave
David Klinkebiel
Judith K Christman
Janos Zempleni
University of Nebraska–Lincoln · USSaint Louis University · USUniversity of Nebraska Medical Center · USNebraska Medical Center · USUniversity of Oklahoma Health Sciences Center · US

Funding

Vitamin-dependent modifications of histonesR01DK063945 · NIDDK · UNIVERSITY OF NEBRASKA LINCOLN · PI ZEMPLENI, JANOS · 2004 to 2011
$2.3M
Epigenetic effects of biotin on activation of endogenous viral sequencesR21ES015206 · NIEHS · UNIVERSITY OF NEBRASKA LINCOLN · PI ZEMPLENI, JANOS · 2006 to 2007
$396k
NIDDK NIH HHS DK 063945NIDDK NIH HHS R01 DK063945NIEHS NIH HHS ES 015206NIEHS NIH HHS R21 ES015206
6 · The paper itself

Abstract

Transposable elements such as long terminal repeats (LTR) constitute approximately 45% of the human genome; transposition events impair genome stability. Fifty-four promoter-active retrotransposons have been identified in humans. Epigenetic mechanisms are important for transcriptional repression of retrotransposons, preventing transposition events, and abnormal regulation of genes. Here, we demonstrate that the covalent binding of the vitamin biotin to lysine-12 in histone H4 (H4K12bio) and lysine-9 in histone H2A (H2AK9bio), mediated by holocarboxylase synthetase (HCS), is an epigenetic mechanism to repress retrotransposon transcription in human and mouse cell lines and in primary cells from a human supplementation study. Abundance of H4K12bio and H2AK9bio at intact retrotransposons and a solitary LTR depended on biotin supply and HCS activity and was inversely linked with the abundance of LTR transcripts. Knockdown of HCS in Drosophila melanogaster enhances retrotransposition in the germline. Importantly, we demonstrated that depletion of H4K12bio and H2AK9bio in biotin-deficient cells correlates with increased production of viral particles and transposition events and ultimately decreases chromosomal stability. Collectively, this study reveals a novel diet-dependent epigenetic mechanism that could affect cancer risk.

Indexed as

DNA Transposable ElementsAdultAnimalsBiotinBiotinylationCarbon-Nitrogen LigasesCell LineChromosome AberrationsCytosineDietary SupplementsDNA MethylationDrosophila melanogasterEpigenesis, GeneticFemaleHistonesHumansBiotinCarbon-Nitrogen LigasesCytosineDNA Transposable ElementsHistonesholocarboxylase synthetasesRepressor Proteins

Identifiers

PMID19022951
PMCPMC2678950
OpenAlexW2131617865

What OpenQuestion holds

Textmetadata
LicenceTDM
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.