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Related Concept Videos

Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
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...
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

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Proximity Ligand Assay to Localize Proteins in DNA Damage Sites
09:39

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Pseudo-DNA damage response in senescent cells.

Tatyana V Pospelova1, Zoya N Demidenko, Elena I Bukreeva

  • 1Institute of Cytology, Russian Academy of Sciences, St. Petersburg, Russia. tvpgroup@mail.ru

Cell Cycle (Georgetown, Tex.)
|December 1, 2009
PubMed
Summary
This summary is machine-generated.

Cellular senescence can occur without DNA damage, activating a DNA damage response (DDR) pathway. This atypical DDR, observed in senescent cells, may indicate general over-activation.

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Area of Science:

  • Cellular biology
  • Molecular biology
  • Aging research

Background:

  • Cellular senescence is traditionally understood as a response to DNA damage.
  • The role of DNA damage response (DDR) pathways in senescence is a key area of research.

Purpose of the Study:

  • To investigate whether cellular senescence can be induced without detectable DNA breaks.
  • To characterize the nature of the DNA damage response (DDR) in senescent cells lacking DNA damage.

Main Methods:

  • Induction of cellular senescence using non-damaging agents (sodium butyrate) and gene expression (p21, p16).
  • Assessment of DNA damage markers (gammaH2AX foci, 53BP1, comet assay) and DDR proteins (p-ATM).
  • Inhibition of senescence using rapamycin (mTOR inhibitor) and evaluation of its effect on DDR markers.

Main Results:

  • Cellular senescence was induced by non-DNA damaging agents and gene expression without detectable DNA breaks.
  • Senescent cells exhibited DDR components like gammaH2AX foci and p-ATM, but lacked 53BP1 accumulation and showed negative comet assay results.
  • Rapamycin treatment reduced gammaH2AX foci formation, suggesting a link between mTOR signaling and DDR activation in senescence.

Conclusions:

  • Cellular senescence can activate an atypical DDR pathway in the absence of detectable DNA damage.
  • The observed DDR in senescent cells may represent a 'pseudo-DDR' phenomenon.
  • Pseudo-DDR could serve as a biomarker for the general over-activation state of senescent cells.