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Related Concept Videos

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 Regulation01:37

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...
Phase II Reactions: Methylation Reactions01:17

Phase II Reactions: Methylation Reactions

Methylation is a phase II biotransformation process involving the attachment of a methyl group to a substrate. Enzymes known as methyltransferases orchestrate this reaction.
The mechanism of methylation unfolds in two stages. The first stage sees a methyltransferase enzyme facilitating the transfer of a methyl group from S-adenosylmethionine (SAM) to the substrate, forming S-adenosylhomocysteine (SAH). The second stage involves further metabolism of SAH into homocysteine, which can be recycled...
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...
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...
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...

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Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
09:42

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Published on: September 7, 2017

LSH and G9a/GLP complex are required for developmentally programmed DNA methylation.

Kevin Myant1, Ausma Termanis, Arvind Y M Sundaram

  • 1Wellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh EH9 3JR, United Kingdom.

Genome Research
|December 15, 2010
PubMed
Summary

The chromatin remodeler LSH (HELLS gene) is crucial for maintaining DNA methylation patterns in mammalian genes. Its absence leads to widespread gene misexpression, highlighting LSH

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Area of Science:

  • Epigenetics
  • Molecular Biology
  • Genomics

Background:

  • The lymphoid-specific helicase (LSH) protein, encoded by the Hells gene, is a member of the SNF2 family of chromatin remodeling ATPases.
  • LSH is known to be essential for DNA methylation of repetitive elements in the mammalian genome.
  • Its role in regulating DNA methylation and gene expression at protein-coding gene promoters is less understood.

Purpose of the Study:

  • To investigate genome-wide DNA methylation patterns at gene promoters in the absence of LSH.
  • To determine the impact of LSH deficiency on gene expression.
  • To elucidate the mechanism by which LSH regulates DNA methylation and gene silencing during cellular differentiation.

Main Methods:

  • Genome-wide DNA methylation analysis in Hells(-/-) mouse embryonic fibroblasts (MEFs) and wild-type MEFs.
  • Gene expression profiling of Hells(-/-) MEFs.
  • Analysis of the interaction between LSH and the G9a/GLP histone methyltransferase complex.

Main Results:

  • Loss of LSH results in significant DNA hypomethylation at approximately 20% of normally methylated promoter sequences.
  • A large number of genes exhibit misexpression in Hells(-/-) MEFs.
  • LSH cooperates with the G9a/GLP complex to establish and maintain DNA methylation and gene silencing at specific promoters, with G9a recruitment impaired in LSH-deficient cells.

Conclusions:

  • LSH is critical for establishing and maintaining DNA methylation at a subset of gene promoters, impacting gene expression during cellular differentiation.
  • LSH facilitates de novo DNA methylation events associated with embryonic lineage commitment.
  • LSH acts in concert with the G9a/GLP complex to ensure stable gene silencing through promoter DNA methylation during differentiation.