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DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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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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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.
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The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
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Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay
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Detecting ATM-dependent chromatin modification in DNA damage response.

Durga Udayakumar1, Nobuo Horikoshi, Lopa Mishra

  • 1Department of Radiation Oncology, Houston Methodist Research Institute, Houston, TX, 77030, USA.

Methods in Molecular Biology (Clifton, N.J.)
|April 2, 2015
PubMed
Summary

The ataxia-telangiectasia mutated (ATM) gene product regulates DNA damage response and chromatin modification. This review explores ATM

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Area of Science:

  • Genetics
  • Molecular Biology
  • Biochemistry

Background:

  • The ataxia-telangiectasia mutated (ATM) gene product is crucial for DNA repair and cell cycle control.
  • ATM belongs to the PI3K-like protein kinase (PIKKs) family and is activated by DNA double-strand breaks (DSBs).
  • ATM plays a role in neurodegeneration, immunodeficiency, and cancer when its function is lost or mutated.

Purpose of the Study:

  • To review the role of ATM and associated proteins in chromatin modification following DNA damage.
  • To summarize approaches used to understand ATM's regulation by chromatin modifications.

Main Methods:

  • Review of existing literature on ATM activation and function.
  • Analysis of studies investigating ATM's interaction with chromatin modifications.
  • Summary of experimental approaches to discern ATM's role in DNA damage response.

Main Results:

  • ATM activation is tightly regulated by chromatin modifications.
  • ATM is detected at DNA damage sites and its activation involves autophosphorylation and dissociation of dimers.
  • Heat shock can activate ATM independently of DNA breaks.

Conclusions:

  • ATM is a key component of the DNA damage sensing machinery.
  • Chromatin modifications play a significant role in regulating ATM activation.
  • Understanding ATM's role in chromatin modification is vital for comprehending its function in DNA repair and disease.