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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

3.0K
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...
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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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Heterochromatin02:38

Heterochromatin

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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 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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Abnormal Proliferation02:23

Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Nucleosome Remodeling02:54

Nucleosome Remodeling

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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
Nucleosome remodeling complex
Eukaryotic cells have specialized enzymes called ATP-dependent nucleosome remodeling enzymes. These enzymes...
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Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

7.3K
The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
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Fractionation for Resolution of Soluble and Insoluble Huntingtin Species
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Accelerated epigenetic aging in Huntington's disease involves polycomb repressive complex 1.

Baptiste Brulé1,2,3, Rafael Alcalá-Vida1,2,3,4, Noémie Penaud1,2,3

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Area of Science:

  • Neuroscience
  • Epigenetics
  • Genetics

Background:

  • Physiological aging leads to epigenetic changes, compromising cellular identity and de-repressing developmental genes.
  • Huntington's disease (HD) is a neurodegenerative disorder affecting vulnerable neurons.
  • Epigenetic alterations are implicated in the pathogenesis of neurodegenerative diseases.

Purpose of the Study:

  • To investigate the epigenomic landscape of vulnerable neurons in mouse models of Huntington's disease.
  • To identify epigenetic mechanisms underlying accelerated aging in HD-affected neurons.
  • To explore the role of Polycomb Repressive Complexes (PRC1 and PRC2) in HD pathogenesis.

Main Methods:

  • Cell-type-specific multi-omics analysis.
  • Temporal analysis across three disease stages in mouse models.
  • Utilized FANS-CUT&Tag for epigenomic profiling.
  • Investigated histone modifications and Polycomb Repressive Complex (PRC) activity.

Main Results:

  • Accelerated de-repression of developmental genes in HD striatal neurons.
  • Observed histone re-acetylation and depletion of H2AK119ub and H3K27me3 marks.
  • Identified a PRC1-dependent reactivation of bivalent developmental transcription factors.
  • Demonstrated PRC1 paralog switching, altering isoform expression in HD neurons.

Conclusions:

  • HD striatal neurons exhibit PRC1-dependent accelerated epigenetic aging.
  • Epigenetic dysregulation, particularly involving PRC1, contributes to HD pathogenesis.
  • Targeting PRC1 may offer therapeutic strategies for Huntington's disease.