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Updated: Aug 15, 2025
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An Inexpensive, Scalable Behavioral Assay for Measuring Ethanol Sedation Sensitivity and Rapid Tolerance in Drosophila
Published on: April 15, 2015
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Chromatin modifier developmental pluripotency associated factor 4 (DPPA4) is a candidate gene for alcohol-induced
P Auvinen1, J Vehviläinen1, H Marjonen1
1Environmental Epigenetics Laboratory, Department of Medical and Clinical Genetics, Medicum, University of Helsinki, 00290, Helsinki, Finland.
BMC Medicine
|December 29, 2022
Summary
Early alcohol exposure can epigenetically alter embryonic development, leading to developmental disorders. This study identifies candidate genes and biomarkers for prenatal alcohol exposure, highlighting placental tissue
Area of Science:
- Developmental Biology
- Epigenetics
- Toxicology
Background:
- Prenatal alcohol exposure (PAE) causes fetal alcohol spectrum disorder (FASD), a complex condition with variable neurodevelopmental and physical defects.
- Epigenetic alterations induced by early alcohol exposure are hypothesized to disrupt embryonic developmental programming, leading to FASD.
- Unique biological samples from newborns exposed to alcohol and controls were collected to investigate FASD etiology.
Purpose of the Study:
- To investigate the epigenetic mechanisms underlying developmental disorders caused by prenatal alcohol exposure.
- To identify candidate genes and potential biomarkers associated with PAE.
- To explore the effects of early alcohol exposure on embryonic and extraembryonic cells.
Main Methods:
- Genome-wide DNA methylation and gene expression analyses were performed on placental tissues.
- DNA methylation changes were assessed in white blood cells and buccal epithelial cells to evaluate biomarker potential.
- Human embryonic stem cells (hESCs) and differentiated cells were exposed to alcohol in vitro to model early developmental effects.
Main Results:
- Significantly decreased DNA methylation was observed in DPPA4, FOXP2, and TACR3 regulatory regions in early alcohol-exposed placentas.
- Alcohol exposure in vitro altered the regulation of DPPA2 in hESCs, with decreased DNA methylation observed in differentiated mesodermal and ectodermal cells.
- Genes with alcohol-associated DNA methylation changes in placenta and hESCs were predominantly linked to neurodevelopmental pathways.
Conclusions:
- Early alcohol exposure impacts human embryonic and extraembryonic cells through epigenetic modifications.
- Candidate genes for alcohol-induced developmental disorders and potential biomarkers for PAE were identified.
- Placental tissue is a valuable resource for analyzing the effects of the prenatal environment on human development.
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