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Related Concept Videos

Histone Modification02:32

Histone Modification

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 deacetylase,...
Histone Modification02:32

Histone Modification

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 deacetylase,...
Spreading of Chromatin Modifications02:25

Spreading of Chromatin Modifications

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 is an enzyme that can...
Inheritance of Chromatin Structures03:17

Inheritance of Chromatin Structures

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 DNA...
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...
Role of Neurotransmitters in Memory01:23

Role of Neurotransmitters in Memory

Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
 Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is critical for...

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Related Experiment Video

Updated: Jun 15, 2026

Quantification of Global Histone Post Translational Modifications Using Intranuclear Flow Cytometry in Isolated Mouse Brain Microglia
07:10

Quantification of Global Histone Post Translational Modifications Using Intranuclear Flow Cytometry in Isolated Mouse Brain Microglia

Published on: September 15, 2023

Histone methylation regulates memory formation.

Swati Gupta1, Se Y Kim, Sonja Artis

  • 1Evelyn F. McKnight Brain Institute, Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|March 12, 2010
PubMed
Summary
This summary is machine-generated.

Histone methylation, specifically H3K4 trimethylation, is crucial for long-term memory consolidation in the hippocampus. This epigenetic modification plays a key role in forming contextual fear memories.

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Purification of H3 and H4 Histone Proteins and the Quantification of Acetylated Histone Marks in Cells and Brain Tissue
09:43

Purification of H3 and H4 Histone Proteins and the Quantification of Acetylated Histone Marks in Cells and Brain Tissue

Published on: November 30, 2018

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Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
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Purification of H3 and H4 Histone Proteins and the Quantification of Acetylated Histone Marks in Cells and Brain Tissue
09:43

Purification of H3 and H4 Histone Proteins and the Quantification of Acetylated Histone Marks in Cells and Brain Tissue

Published on: November 30, 2018

Area of Science:

  • Neuroscience
  • Epigenetics
  • Molecular Biology

Background:

  • Histone modifications like phosphorylation and acetylation are vital for synaptic plasticity and memory.
  • The role of histone methylation in memory formation remains less understood.

Purpose of the Study:

  • To investigate the contribution of histone methylation to memory formation in the adult hippocampus.
  • To explore the specific roles of H3K4 trimethylation and H3K9 dimethylation in contextual fear conditioning.

Main Methods:

  • Analyzing histone methylation levels (H3K4me3, H3K9me2) in the hippocampus after contextual fear conditioning.
  • Assessing contextual fear conditioning in mice deficient in the H3K4-specific methyltransferase Mll.
  • Investigating the effects of histone deacetylase inhibition (sodium butyrate) on histone methylation patterns.
  • Examining gene promoter methylation and MeCP2 binding at Zif268 and bdnf loci.

Main Results:

  • H3K4 trimethylation (H3K4me3) upregulated 1 hour after fear conditioning; H3K9 dimethylation (H3K9me2) increased at 1 hour and decreased at 24 hours.
  • Mice lacking Mll showed impaired contextual fear conditioning.
  • Inhibition of HDACs increased H3K4me3 and decreased H3K9me2.
  • Fear learning induced H3K4me3 at Zif268 and bdnf promoters, with altered DNA methylation and MeCP2 binding.

Conclusions:

  • Histone methylation is actively regulated in the hippocampus during memory formation.
  • Histone methylation, particularly H3K4me3, is essential for the long-term consolidation of contextual fear memories.
  • Epigenetic modifications at specific gene loci are involved in the molecular mechanisms of memory consolidation.