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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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Background and Environment Affect Phenotype02:27

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Although the genetic makeup of an organism plays a major role in determining the phenotype, there are also several environmental factors, such as temperature, oxygen availability, presence of mutagens, that can alter an organism’s phenotype.
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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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Related Experiment Video

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Using Caenorhabditis elegans for Studying Trans- and Multi-Generational Effects of Toxicants
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Epigenetic programming alterations in alligators from environmentally contaminated lakes.

Louis J Guillette1, Benjamin B Parrott1, Eric Nilsson2

  • 1Department of Obstetrics and Gynecology, Marine Biomedicine and Environmental Sciences Program, Medical University of South Carolina, Hollings Marine Laboratory, Charleston, SC 29412, USA.

General and Comparative Endocrinology
|April 16, 2016
PubMed
Summary

Environmental contaminants in Florida lakes are linked to epigenetic changes in alligators. DNA methylation alterations in red blood cells may serve as biomarkers for assessing environmental exposures and health impacts.

Keywords:
AlligatorDNA methylationEndocrine disruptorsEnvironmental epigenetics

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Area of Science:

  • Environmental epigenetics
  • Wildlife toxicology
  • Alligator reproductive health

Background:

  • Florida alligators exhibit reproductive health issues linked to environmental quality and contaminant exposure.
  • Many environmental contaminants disrupt endocrine signaling pathways.
  • Epigenetic modifications, such as DNA methylation, are potential mediators of these environmentally induced health abnormalities.

Purpose of the Study:

  • To investigate the association between environmental conditions and epigenetic status in alligators.
  • To identify potential epigenetic biomarkers for environmental exposures and health impacts.

Main Methods:

  • Red blood cells (RBCs) from adult male alligators from three Florida lakes with varying contamination levels were analyzed.
  • DNA methylation patterns were assessed using methylated DNA immunoprecipitation coupled with genome-wide tiling array analysis (MeDIP-Chip).
  • Differential DNA methylation regions (DMRs) were identified by comparing alligator populations from contaminated sites (Lake Apopka, Merritt Island) to a relatively pristine site (Lake Woodruff).

Main Results:

  • Significant alterations in the DNA methylome were observed in alligators from contaminated sites compared to the pristine site.
  • Numerous differential DNA methylation regions (DMRs) were identified, primarily in CpG-poor regions (CpG deserts).
  • Identified DMRs were associated with genes relevant to endocrine function, suggesting a link between environmental contaminants, epigenetics, and endocrine disruption.

Conclusions:

  • Environmental quality and contaminant exposures are associated with epigenetic programming in alligators.
  • Epigenetic alterations, specifically in DNA methylation, may serve as valuable biomarkers for assessing environmental exposures and their health consequences in wildlife populations.
  • This study highlights the role of epigenetics in mediating the impact of environmental stressors on alligator health.