Evidence map›Paper›PMID 20084100›Full record

ArticlePLoS genetics2010

Maternal ethanol consumption alters the epigenotype and the phenotype of offspring in a mouse model.

Nina Kaminen-Ahola, Arttu Ahola, Murat Maga, Kylie-Ann Mallitt, Paul Fahey, Timothy C Cox, Emma Whitelaw, Suyinn Chong

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed, 2 pooled it
40.7field-weighted citation impact, top 1% 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

151 citing papers in PubMed, 2 syntheses or guidelines pooled it, 342 citations in OpenAlex.

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  19. Mitigating the detrimental developmental impact of early fetal alcohol exposure using a maternal methyl donor-enriched diet.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  20. Article

91 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

8 authors at 4 institutions in 3 countries.

Nina Kaminen-AholaDivision of Genetics and Population Health, Queensland Institute of Medical Research, Herston, Australia.
Arttu Ahola
Murat Maga
Kylie-Ann Mallitt
Paul Fahey
Timothy C Cox
Emma Whitelaw
Suyinn Chong
QIMR Berghofer Medical Research Institute · AUUniversity of Washington · USGriffith University · AUUniversity of Helsinki · FI

Funding

Cross-Cultural Assessment of FASDU24AA014811 · NIAAA · SAN DIEGO STATE UNIVERSITY · PI EDWARD P RILEY · 2003 to 2026
$13.1M
NIAAA NIH HHS U24 AA014811
6 · The paper itself

Abstract

Recent studies have shown that exposure to some nutritional supplements and chemicals in utero can affect the epigenome of the developing mouse embryo, resulting in adult disease. Our hypothesis is that epigenetics is also involved in the gestational programming of adult phenotype by alcohol. We have developed a model of gestational ethanol exposure in the mouse based on maternal ad libitum ingestion of 10% (v/v) ethanol between gestational days 0.5-8.5 and observed changes in the expression of an epigenetically-sensitive allele, Agouti viable yellow (A(vy)), in the offspring. We found that exposure to ethanol increases the probability of transcriptional silencing at this locus, resulting in more mice with an agouti-colored coat. As expected, transcriptional silencing correlated with hypermethylation at A(vy). This demonstrates, for the first time, that ethanol can affect adult phenotype by altering the epigenotype of the early embryo. Interestingly, we also detected postnatal growth restriction and craniofacial dysmorphology reminiscent of fetal alcohol syndrome, in congenic a/a siblings of the A(vy) mice. These findings suggest that moderate ethanol exposure in utero is capable of inducing changes in the expression of genes other than A(vy), a conclusion supported by our genome-wide analysis of gene expression in these mice. In addition, offspring of female mice given free access to 10% (v/v) ethanol for four days per week for ten weeks prior to conception also showed increased transcriptional silencing of the A(vy) allele. Our work raises the possibility of a role for epigenetics in the etiology of fetal alcohol spectrum disorders, and it provides a mouse model that will be a useful resource in the continued efforts to understand the consequences of gestational alcohol exposure at the molecular level.

Indexed as

Models, AnimalAlcohol DrinkingAnimalsEmbryonic DevelopmentEpigenesis, GeneticEthanolFemaleGene Expression Regulation, DevelopmentalGene SilencingHumansMaleMaternal ExposureMiceMice, Inbred C57BLPedigreePregnancyEthanol

Identifiers

PMID20084100
PMCPMC2797299
OpenAlexW2061463822

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.