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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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The spindle assembly checkpoint is a molecular surveillance mechanism ensuring the fidelity of chromosome segregation during anaphase. The checkpoint monitors the completion of all the prerequisite steps before chromosome segregation to determine whether the segregation process should proceed or be delayed.
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The Spindle Assembly Checkpoint02:19

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The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
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The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...

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Detection of DNA Double-Stranded Breaks in Mouse Oocytes
07:46

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Published on: June 23, 2023

ATM controls meiotic double-strand-break formation.

Julian Lange1, Jing Pan, Francesca Cole

  • 1Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA.

Nature
|October 18, 2011
PubMed
Summary

The ATM kinase restrains double-strand break (DSB) formation during meiosis by suppressing SPO11 activity. This negative feedback loop prevents excessive DSBs, crucial for preventing meiotic errors and gonadal dysgenesis.

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Area of Science:

  • Genetics
  • Molecular Biology
  • Cell Biology

Background:

  • Meiotic recombination is initiated by programmed double-strand breaks (DSBs) formed by SPO11.
  • Adequate DSB formation is essential for homologous chromosome pairing and segregation.
  • Excessive or improperly repaired DSBs can lead to meiotic arrest or mutations.

Purpose of the Study:

  • To investigate the mechanisms controlling the number of meiotic double-strand breaks (DSBs).
  • To determine the role of ATM kinase in regulating DSB formation during meiosis.
  • To elucidate the molecular basis for gonadal dysgenesis in ATM-deficient individuals.

Main Methods:

  • Analysis of SPO11-oligonucleotide complexes in wild-type and ATM-deficient mouse spermatocytes.
  • Genetic manipulation of SPO11 protein levels in the context of ATM mutation.
  • Investigating the activation of ATM kinase in response to DNA damage.

Main Results:

  • Spermatocytes lacking ATM exhibit a tenfold increase in SPO11-oligonucleotide complexes, indicating elevated DSB formation.
  • ATM deficiency renders SPO11-oligonucleotide levels sensitive to changes in SPO11 protein levels.
  • ATM kinase activation by DSBs appears to suppress further DSB formation.

Conclusions:

  • ATM acts as a negative regulator of meiotic DSB formation through a feedback loop.
  • This ATM-mediated control of DSBs is essential for preventing excessive DNA breaks and ensuring proper meiosis.
  • The findings provide a molecular explanation for gonadal dysgenesis in ataxia telangiectasia patients.