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Related Concept Videos

Epigenetic Regulation01:37

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 Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Genomic Imprinting and Inheritance02:30

Genomic Imprinting and Inheritance

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.
The expression of some genes depends on which parent passed the gene to the offspring, through a phenomenon known as...
Methods of Nuclear Reprogramming01:24

Methods of Nuclear Reprogramming

Nuclear reprogramming is a process of transforming one cell type into an unrelated cell type by epigenetic changes that alter the cell’s original gene expression pattern. Such epigenetic changes force cells to express a different set of genes, which play a significant role in inducing transformation into other cell types. Nuclear reprogramming offers applications in reproductive cloning for livestock propagation and regenerative medicine — developing patient-specific cells for injury repair.
Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
Compact chromatin makes reprogramming difficult. Enzymes, such as histone demethylases and acetyltransferases, are often added during reprogramming to loosen the chromatin, making the DNA more accessible to transcription factors. Molecules that inhibit histone...

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Related Experiment Video

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Instrumentation of Near-term Fetal Sheep for Multivariate Chronic Non-anesthetized Recordings
14:40

Instrumentation of Near-term Fetal Sheep for Multivariate Chronic Non-anesthetized Recordings

Published on: October 25, 2015

Epigenetic regulation and fetal programming.

Christine Gicquel1, Assam El-Osta, Yves Le Bouc

  • 1Epigenetics in Human Health and Disease, Baker Medical Research Institute, 75 Commercial Road, Melbourne, 3004 Victoria, Australia. christine.gicquel@baker.edu.au

Best Practice & Research. Clinical Endocrinology & Metabolism
|February 19, 2008
PubMed
Summary
This summary is machine-generated.

Fetal programming links early life exposures to later disease risk. Epigenetic changes in genes may explain how these environmental signals impact long-term health outcomes.

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Area of Science:

  • Developmental biology
  • Epigenetics
  • Public health

Background:

  • Fetal programming explores how early life environmental and nutritional signals influence later-life health.
  • Early studies linked poor fetal growth to chronic adult diseases like cardiovascular and metabolic conditions.
  • Adverse long-term effects can occur even without obvious fetal growth impacts, stemming from a mismatch in early vs. later life environments.

Purpose of the Study:

  • To elucidate the mechanisms underlying fetal programming and its long-term health consequences.
  • To investigate the role of epigenetic modifications in mediating the effects of early life exposures.
  • To identify potential biomarkers for early detection of disease risk.

Main Methods:

  • Review of experimental data in rodents.
  • Analysis of recent human observational studies.
  • Focus on epigenetic changes in regulatory and growth-related genes.

Main Results:

  • Environmental signals during early life can lead to adverse long-term effects independently of fetal growth.
  • Epigenetic alterations in specific genes are suggested as a key mechanism in fetal programming.
  • A mismatch between early and later life environments is a critical factor in adverse outcomes.

Conclusions:

  • Understanding fetal programming mechanisms, particularly epigenetic changes, is crucial for identifying high-risk infants.
  • Biomarkers for detecting at-risk infants could be developed through further research.
  • Improved knowledge will facilitate the creation of preventive and therapeutic strategies for adult-onset diseases.