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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...
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

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Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.

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CCCTC-binding factor activates PARP-1 affecting DNA methylation machinery.

Tiziana Guastafierro1, Barbara Cecchinelli, Michele Zampieri

  • 1Department of Cellular Biotechnology and Haematology, University La Sapienza, Piazzale Aldo Moro 5, 00161 Rome, Italy.

The Journal of Biological Chemistry
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CCCTC-binding factor (CTCF) overexpression induces poly(ADP-ribosyl)ation (PAR), inhibiting DNA methyltransferase 1 (DNMT1) activity and causing genome-wide hypomethylation. This highlights CTCF

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Area of Science:

  • Epigenetics
  • Molecular Biology
  • Genomics

Background:

  • DNA methylation patterns are crucial epigenetic regulators.
  • Poly(ADP-ribosyl)ation (PAR) influences DNA methylation control.
  • ADP-ribose polymers (PARs) inhibit DNA methyltransferase 1 (DNMT1) activity.

Purpose of the Study:

  • To investigate the role of CCCTC-binding factor (CTCF) in regulating poly(ADP-ribosyl)ation (PAR) and its impact on DNA methylation.
  • To elucidate the mechanism by which CTCF influences the interplay between PARP-1 and DNMT1.
  • To determine the consequences of CTCF-induced PAR accumulation on genome-wide methylation.

Main Methods:

  • Transient ectopic overexpression of CTCF in L929 mouse fibroblasts.
  • Measurement of PAR accumulation, PARP-1, and CTCF poly(ADP-ribosyl)ation.
  • Assessment of DNA methyltransferase activity and genome-wide methylation status.
  • In vitro studies on CTCF's ability to activate PARP-1 automodification.

Main Results:

  • CTCF overexpression induces significant PAR accumulation and poly(ADP-ribosyl)ation of PARP-1 and CTCF.
  • Sustained high PAR levels inhibit DNMT1 activity, leading to diffuse genomic hypomethylation.
  • CTCF activates PARP-1 automodification in vitro, independent of DNA strand breaks.
  • CTCF does not directly inhibit DNMT1; rather, poly(ADP-ribosyl)ated PARP-1 mediates this inhibition.

Conclusions:

  • CTCF plays a critical role in the cross-talk between poly(ADP-ribosyl)ation and DNA methylation.
  • CTCF-induced PARP-1 activation influences DNA methylation machinery, impacting epigenetic regulation.
  • The findings underscore the importance of timely PARP activity reversal for maintaining epigenetic integrity.