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Epigenetic Regulation

Epigenetic Regulation

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...

Epigenetic Regulation

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.

Phase II Reactions: Methylation Reactions

Phase II Reactions: Methylation Reactions

Methylation is a phase II biotransformation process involving the attachment of a methyl group to a substrate. Enzymes known as methyltransferases orchestrate this reaction.
The mechanism of methylation unfolds in two stages. The first stage sees a methyltransferase enzyme facilitating the transfer of a methyl group from S-adenosylmethionine (SAM) to the substrate, forming S-adenosylhomocysteine (SAH). The second stage involves further metabolism of SAH into homocysteine, which can be recycled...

Spontaneous and Induced Mutations

Spontaneous and Induced Mutations

Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).

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Related Experiment Video

Updated: Jun 26, 2026

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images

Published on: September 7, 2017

Rapid DNA methylation changes after exposure to traffic particles.

Andrea Baccarelli¹, Robert O Wright, Valentina Bollati

¹Laboratory of Environmental Epigenetics, Department of Environmental and Occupational Health, University of Milan, Via San Barnaba 8, 20122 Milan, Italy. andrea.baccarelli@unimi.it

American Journal of Respiratory and Critical Care Medicine

|January 13, 2009

Summary

Exposure to traffic particles, like black carbon and PM2.5, was linked to decreased DNA methylation in repetitive elements. This finding suggests a potential mechanism for how air pollution impacts cardiovascular health.

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Analysis of the Ambient Particulate Matter-induced Chromosomal Aberrations Using an In Vitro System

Analysis of the Ambient Particulate Matter-induced Chromosomal Aberrations Using an In Vitro System

Published on: December 21, 2016

Area of Science:

Environmental Epigenetics
Cardiovascular Epidemiology
Toxicology

Background:

Particulate air pollution is linked to increased cardiovascular disease (CVD) risk, hospitalizations, and mortality.
Lower blood DNA methylation is associated with CVD risk factors like oxidative stress, aging, and atherosclerosis.

Purpose of the Study:

To investigate if exposure to particulate air pollution influences DNA methylation levels in human repetitive DNA sequences.
To examine the association between specific pollutants (black carbon, PM2.5, sulfate) and methylation of LINE-1 and Alu elements.

Main Methods:

Quantitative polymerase chain reaction-pyrosequencing was used to measure DNA methylation of LINE-1 and Alu elements in 1,097 blood samples.
Covariate-adjusted mixed models analyzed associations between pollutants and methylation across various time windows (4 hours to 7 days).
Standardized regression coefficients (beta) quantified the change in DNA methylation per standard deviation increase in pollutant exposure.

Main Results:

DNA methylation of repetitive elements showed variation with time-related factors (day of week, season).
Increased exposure to black carbon and PM2.5 was significantly associated with decreased LINE-1 methylation.
Black carbon, a marker for traffic particles, was the primary pollutant linked to LINE-1 methylation changes in two-pollutant models.

Conclusions:

Exposure to traffic-related particles is associated with reduced repetitive element DNA methylation.
Further research is needed to determine if this epigenetic modification mediates the health effects of air pollution exposure.