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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying...
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Related Experiment Video

Updated: Mar 3, 2026

Correlating Gene-specific DNA Methylation Changes with Expression and Transcriptional Activity of Astrocytic KCNJ10 Kir4.1
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DNA Methylation program in normal and alcohol-induced thinning cortex.

Nail Can Öztürk1, Marisol Resendiz2, Hakan Öztürk3

  • 1Anatomy Department of Mersin University, School of Medicine, Mersin, 33343, Turkey; Department of Anatomy and Cellular Biology, Indiana University School of Medicine, 635 Barnhill Dr., MS5035, Indianapolis, IN, 46202, USA.

Alcohol (Fayetteville, N.Y.)
|April 24, 2017
PubMed
Summary
This summary is machine-generated.

Fetal alcohol spectrum disorders (FASD) disrupt brain development. This study shows alcohol exposure in mice alters DNA methylation, impacting cortical thinning and neurodevelopment, raising questions about epigenetic influences.

Keywords:
EpigeneticsFetal Alcohol Spectrum Disorders (FASD)Neurodevelopmental deficitNeuroepigeneticsNeurogenesis

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Epigenetics

Background:

  • Fetal alcohol spectrum disorders (FASD) are characterized by cerebral underdevelopment.
  • The precise mechanisms driving cortical neurodevelopmental deficits in FASD remain unclear.
  • DNA methylation plays a crucial role in regulating early development and gene expression.

Purpose of the Study:

  • To investigate the role of DNA methylation in alcohol-induced cortical thinning in a mouse model of FASD.
  • To assess the impact of prenatal alcohol exposure on cortical neuroanatomy, neural phenotypes, and epigenetic markers.

Main Methods:

  • C57BL/6 mice were exposed to an alcohol liquid diet during critical embryonic development (E7-16).
  • Cortical neuroanatomy, neuroepithelial proliferation, and neuronal migration/maturity were analyzed at E17.
  • Epigenetic markers, including 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC), were quantified using methyl-DNA assays, Western blot, and immunohistochemistry.

Main Results:

  • Prenatal alcohol exposure significantly deterred cortical thickness, neuroepithelial proliferation, and neuronal migration and maturity at E17.
  • In utero alcohol exposure severely disrupted DNA methylation patterns (5mC and 5hmC), which are critical for normal embryonic cortical development.
  • A strong correlation was observed between cortical thinning and the disruption of the DNA methylation program.

Conclusions:

  • Fetal alcohol exposure profoundly disrupts the dynamic DNA methylation program essential for embryonic cortical development.
  • These epigenetic disruptions occur concurrently with structural and molecular developmental abnormalities characteristic of FASD.
  • Future research should explore whether epigenetic modifications guide neurodevelopment or if developmental conditions dictate epigenetic changes in alcohol-induced teratogenesis.