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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.
X-chromosome...
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Gene-Environment Interactions01:20

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Gene expression is a dynamic process that is significantly influenced by environmental factors. This interaction underlies the complex nature of biological development and the phenotypic differences observed among individuals, even among those with identical genetic makeups. Factors such as radiation, temperature, behavior, nutrition, and stress play pivotal roles in determining how genes are expressed. The concept of the reaction range is central to understanding this interaction. It posits...
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Inheritance of Chromatin Structures03:17

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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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Histone Modification02:32

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The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
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Diploid organisms inherit genetic material through chromosomes from both parents. Copies of the same gene are known as alleles. In most cases, both alleles are simultaneously expressed and allow various cellular processes to function optimally. If one of the alleles is missing or mutated, the expression of the other allele can compensate; however, this is not true for all genes.
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Nucleosome Remodeling02:54

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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
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Related Experiment Video

Updated: Jul 2, 2025

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
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DNA methylation-environment interactions in the human genome.

Rachel A Johnston1,2,3, Katherine A Aracena4, Luis B Barreiro4,5,6

  • 1Department of Evolutionary Anthropology, Duke University, Durham, United States.

Elife
|February 26, 2024
PubMed
Summary

DNA methylation patterns influence gene regulation and cellular responses to environmental factors like interferon alpha. However, sites linked to early life adversity do not show increased regulatory function.

Keywords:
IFNAMPRAbiological embeddingchromosomesearly life adversityepigenomegene expressionhumanmethylation

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Area of Science:

  • Epigenetics and Genomics
  • Molecular Biology
  • Systems Biology

Background:

  • The massively parallel reporter assay (mSTARR-seq) previously enabled simultaneous testing of enhancer activity and DNA methylation-dependent enhancer activity for millions of genomic loci.
  • DNA methylation is a key epigenetic mechanism influencing gene regulation and cellular function, with potential implications for environmental interactions.

Purpose of the Study:

  • To apply mSTARR-seq to a near-genome-wide scale, interrogating millions of CpG sites.
  • To investigate the regulatory capacity of DNA methylation and its interaction with cellular environments, particularly in response to interferon alpha (IFNA).
  • To assess whether DNA methylation patterns associated with early life adversity predict functional regulatory roles.

Main Methods:

  • Application of mSTARR-seq to query nearly the entire human genome, covering CpG sites from common methylation arrays and sequencing methods.
  • Analysis of DNA methylation-dependent regulatory activity in response to IFNA stimulation.
  • Correlation of mSTARR-seq identified methylation-dependent responses with transcriptional responses to influenza virus in human macrophages.

Main Results:

  • Genomic fragments containing CpG sites are enriched for regulatory capacity.
  • Methylation-dependent regulatory activity is sensitive to the cellular environment, with IFNA responses significantly attenuated by methyl marks.
  • Methylation-dependent responses to IFNA predict methylation-dependent transcriptional responses to influenza virus, supporting DNA methylation-environment interactions.
  • No significant enrichment for functional regulatory influence was found for sites previously associated with early life adversity.

Conclusions:

  • Pre-existing DNA methylation patterns can modulate responses to subsequent environmental exposures, aligning with biological embedding principles.
  • Widespread DNA methylation-environment interactions exist, impacting cellular responses to stimuli like IFNA.
  • The functional regulatory impact of DNA methylation is context-dependent and not universally elevated for sites linked to early life adversity.