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Related Concept Videos

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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Histone Modification02:32

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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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Histone Variants at the Centromere02:30

Histone Variants at the Centromere

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Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3...
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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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The Nucleosome Core Particle01:12

The Nucleosome Core Particle

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Nucleosomes are the DNA-histone complex, where the DNA strand is wound around the histone core. The histone core is an octamer containing two copies of H2A, H2B, H3, and H4 histone proteins.
Nucleosomes, paradoxically, perform two opposite functions simultaneously. On the one hand, their primary aim is to protect the delicate DNA strands from physical damage and help achieve a higher compaction ratio. On the other hand, they must allow polymerase enzymes to access histone-bound DNA during...
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Characterizing Histone Post-translational Modification Alterations in Yeast Neurodegenerative Proteinopathy Models
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Alzheimer's Disease and Histone Code Alterations.

Pritika Narayan1, Mike Dragunow2

  • 1School of Biological Sciences and Centre for Brain Research, University of Auckland, Auckland, New Zealand.

Advances in Experimental Medicine and Biology
|May 20, 2017
PubMed
Summary
This summary is machine-generated.

Genome-wide association studies (GWAS) identify Alzheimer's disease (AD) risk variants, often in noncoding DNA. These findings suggest complex genetic and epigenetic factors contribute to both familial and sporadic AD.

Keywords:
EpigeneticsHistone modificationsHuman brain

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Area of Science:

  • Genetics
  • Neuroscience
  • Genomics

Background:

  • Genome-wide association studies (GWAS) have identified numerous Alzheimer's disease (AD) risk variants.
  • Most identified AD risk variants are located in noncoding genomic regions, posing challenges for functional interpretation.
  • Familial Alzheimer's disease (AD) accounts for a small percentage of cases, with known mutations in APP, PSEN1, and PSEN2 explaining a fraction of these.
  • Sporadic AD has a significant genetic component, with a substantial proportion of patients having affected first-degree relatives.
  • APOE E4 polymorphism is a major risk factor for AD, alongside over 20 other identified risk variants.
  • Monozygotic twin studies indicate that both genetic and epigenetic factors likely play a role in AD development.

Purpose of the Study:

  • To review the progress in identifying Alzheimer's disease (AD) risk-associated variants.
  • To highlight the challenges and implications of noncoding variants in AD genetics.
  • To emphasize the combined role of genetic and epigenetic factors in AD pathogenesis.

Main Methods:

  • Review of existing literature on genome-wide association studies (GWAS) for Alzheimer's disease (AD).
  • Analysis of data regarding the location and implications of identified AD risk variants.
  • Synthesis of findings from familial and sporadic AD genetic studies, including twin studies.

Main Results:

  • GWAS have successfully identified numerous AD risk variants.
  • A majority of these variants are in noncoding regions, suggesting novel regulatory elements.
  • Genetic factors, including APOE E4 and other variants, contribute significantly to AD risk.
  • Epigenetic factors are implicated in AD development, as suggested by twin studies.

Conclusions:

  • Identifying functional roles of noncoding AD risk variants is crucial for understanding disease mechanisms.
  • Both common and rare genetic variants, alongside epigenetic modifications, contribute to Alzheimer's disease (AD) etiology.
  • Further research into the interplay of genetic and epigenetic factors is essential for developing effective AD prevention and treatment strategies.