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Related Concept Videos

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...
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.
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...
Maintenance of the ES Cell State01:14

Maintenance of the ES Cell State

The cells of the blastocyst inner cell mass only remain pluripotent for a short time. This state of pluripotency and self-renewal can be maintained in embryonic stem (ES) cell culture by adding specific chemicals or growth factors to ensure the cells can continue dividing and later differentiate into different cell types. In some cases, the cells are grown on a feeder layer of differentiated cells, which provides the growth factors and extracellular matrix components necessary for stem cell...
Heterochromatin02:38

Heterochromatin

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 9th...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...

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Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
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Published on: September 7, 2017

Maintaining the unmethylated state.

Steven S Smith1

  • 1City of Hope, 1500 East Duarte Road, Duarte, CA 91010, USA. ssmith@coh.org.

Clinical Epigenetics
|October 2, 2013
PubMed
Summary
This summary is machine-generated.

Fragile sites prone to non-B DNA structures are epigenetically repaired by helicases and TET dioxygenases, preventing hypermethylation. Impaired helicase function leads to DNA methyltransferase (DNMT) sequestration and altered methylation patterns.

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Published on: January 26, 2018

Area of Science:

  • Epigenetics
  • Genomics
  • Molecular Biology

Background:

  • Fragile sites correlate with hypermethylation sites.
  • Fragile sites feature DNA sequences prone to non-B DNA structure formation.
  • Enzymes like DNA methyltransferase 1 (DNMT1), helicases, and TET dioxygenases are implicated.

Purpose of the Study:

  • To propose a previously unrecognized epigenetic repair cycle.
  • To explain how non-B DNA structures at fragile sites are managed in normal cells.
  • To link helicase and TET dioxygenase activity to maintaining unmethylated states.

Main Methods:

  • The hypothesis predicts that helicase knockdown will increase bisulfite sensitivity and hypermethylation at non-B structures.
  • Global hypomethylation is also predicted upon helicase knockdown.
  • This study focuses on the functional consequences of impaired helicase activity at fragile sites.

Main Results:

  • Knockdown of ATP-dependent and actin-dependent helicases is predicted to cause hypermethylation at non-B structures.
  • Global hypomethylation is expected as a consequence of helicase dysfunction.
  • These results support the role of helicases in preventing aberrant DNA methylation.

Conclusions:

  • Helicases prevent DNA methyltransferases (DNMTs) sequestration at unrepaired non-B DNA structures.
  • Blocked helicase activity leads to DNMT stalling and hypermethylation at fragile sites.
  • This results in localized hypermethylation and global hypomethylation, impacting genome-wide methylation maintenance.