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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...
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

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...
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.
Phosphorylation01:02

Phosphorylation

The addition or removal of phosphate groups from proteins is the most common chemical modification that regulates cellular processes. These modifications can affect the structure, activity, stability, and localization of proteins within cells as well as their interactions with other proteins.
During phosphorylation, protein kinases transfer the terminal phosphate group of ATP to specific amino acid side chains of substrate proteins. Serine, threonine, and tyrosine are the most commonly...
Phosphorylation01:02

Phosphorylation

The addition or removal of phosphate groups from proteins is the most common chemical modification that regulates cellular processes. These modifications can affect the structure, activity, stability, and localization of proteins within cells as well as their interactions with other proteins.
During phosphorylation, protein kinases transfer the terminal phosphate group of ATP to specific amino acid side chains of substrate proteins. Serine, threonine, and tyrosine are the most commonly...

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Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

Phosphatases, DNA damage checkpoints and checkpoint deactivation.

Johanna Heideker1, Ewa T Lis, Floyd E Romesberg

  • 1Department of Chemistry, The Scripps Research Institute, La Jolla, California 92037, USA.

Cell Cycle (Georgetown, Tex.)
|December 14, 2007
PubMed
Summary

Specific phosphatases Pph3, Ptc2, and Ptc3 are crucial for deactivating DNA damage checkpoints in yeast by targeting Rad53. This ensures cells can resume growth after DNA repair.

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Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • DNA damage checkpoints are essential for cell cycle arrest and DNA repair.
  • Ser/Thr kinases like Rad53 (yeast Chk2) activate these checkpoints via phosphorylation.
  • Mechanisms for checkpoint deactivation and cell cycle re-entry are less understood.

Purpose of the Study:

  • To review the roles of phosphatases in DNA damage checkpoint deactivation in Saccharomyces cerevisiae.
  • To focus on the specific functions of Pph3 and PP2C phosphatases (Ptc2, Ptc3) in Rad53 deactivation.

Main Methods:

  • Review of existing literature on DNA damage response pathways in S. cerevisiae.
  • Analysis of the non-redundant roles of specific phosphatases in checkpoint regulation.
  • Discussion of phosphatase specificity towards phosphorylated forms of Rad53.

Main Results:

  • The type 2A phosphatase Pph3 and PP2C phosphatases Ptc2 and Ptc3 play non-redundant roles in deactivating the Rad53 checkpoint.
  • These phosphatases likely recognize distinct phosphorylated forms of Rad53.
  • Individual phosphatases regulate different aspects of the DNA damage checkpoint response.

Conclusions:

  • Specific phosphatases are critical for the timely deactivation of DNA damage checkpoints.
  • Differential regulation by phosphatases allows for a tailored cellular response to DNA damage.
  • Coordinated dephosphorylation facilitates DNA repair and the resumption of cell growth.