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Related Concept Videos

Heterochromatin02:38

Heterochromatin

19.0K
The extent of chromatin compaction can be studied by staining chromatin using specific DNA binding dyes. Under the microscope, the dense-compacted regions that take up more dye are called heterochromatin. Heterochromatin is further classified into two forms – constitutive heterochromatin and facultative heterochromatin.
Constitutive heterochromatin: It is a highly compact region of chromatin that is mostly concentrated in the centromere and telomere. Unlike euchromatin, the amino acid at...
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Spreading of Chromatin Modifications02:25

Spreading of Chromatin Modifications

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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
The writer...
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Euchromatin01:01

Euchromatin

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The extent of chromatin compaction can be studied by staining chromatin using specific DNA binding dyes. Under the microscope, the dense-compacted regions take up more dye, appearing darker, while the less-compact areas take up less dye and appear lighter. Based on the compaction level, chromatins are classified into two primary forms – euchromatin and heterochromatin.
Euchromatin is the less dense region of the chromatin and stains lighter. Euchromatin contains histone H3 extensively...
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Histone Modification02:32

Histone Modification

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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.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone...
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Inheritance of Chromatin Structures03:17

Inheritance of Chromatin Structures

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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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Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

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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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Chromatin Immunoprecipitation of Murine Brown Adipose Tissue
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Persistent Chromatin Modifications Induced by High Fat Diet.

Amy Leung1, Candi Trac1, Juan Du2

  • 1From the Department of Diabetes Complications and Metabolism, Beckman Research Institute, and.

The Journal of Biological Chemistry
|March 24, 2016
PubMed
Summary
This summary is machine-generated.

Diet-induced obesity can cause lasting epigenetic changes in liver chromatin, particularly in C57BL/6J mice. These persistent alterations may contribute to metabolic disorders and offer therapeutic targets.

Keywords:
chromatin modificationchromatin remodelinggene regulationliver metabolismmetabolic diseasemetabolic memory

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Area of Science:

  • Genomics
  • Epigenetics
  • Metabolic Disease

Background:

  • Obesity is a complex, heritable disease influenced by genetics and environment.
  • Formerly obese individuals risk metabolic disorders due to "metabolic memory," similar to diabetic complications.
  • Epigenetic modifications are potential mediators of this metabolic memory.

Purpose of the Study:

  • To investigate the persistence of diet-induced chromatin accessibility changes after diet reversal in mice.
  • To determine if genetic background influences the reversibility of these epigenetic changes.
  • To identify epigenetic mechanisms underlying persistent metabolic changes.

Main Methods:

  • High-fat diet induction and subsequent reversal in C57BL/6J and A/J mouse strains.
  • Chromatin accessibility profiling (e.g., ATAC-seq) in mouse liver tissue.
  • Analysis of transcription factor binding and histone modifications at accessible loci.

Main Results:

  • Diet-induced chromatin accessibility changes were largely persistent in C57BL/6J mice after diet reversal.
  • In contrast, most chromatin changes were transient in A/J mice, highlighting strain-dependent epigenetic memory.
  • Persistent changes in C57BL/6J mice were linked to specific transcription factors and histone modifications.

Conclusions:

  • Epigenetic modifications in liver chromatin can exhibit long-term memory of high-fat diet exposure.
  • Genetic background significantly influences the persistence of diet-induced epigenetic alterations.
  • Persistent epigenetic changes represent potential targets for therapeutic interventions against obesity-related metabolic disorders.