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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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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,...
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Related Experiment Video

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Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
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TopBP1-mediated DNA processing during mitosis.

Irene Gallina1, Signe Korbo Christiansen1, Rune Troelsgaard Pedersen1

  • 1a Department of Biology , University of Copenhagen , Copenhagen N , Denmark.

Cell Cycle (Georgetown, Tex.)
|December 25, 2015
PubMed
Summary

TopBP1 protein is vital for DNA repair during cell division, ensuring genome stability. Our study shows TopBP1 promotes DNA synthesis independently of translesion polymerases, preventing damage transmission to daughter cells.

Keywords:
PCNA ubiquitylationREV1TopBP1fork restartmitosispolymerase ηpost-replicative gapsreplication stresstranslesion synthesis

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Area of Science:

  • Cell Biology
  • Genetics
  • Molecular Biology

Background:

  • Genome integrity is essential for preventing cancer and genetic disorders.
  • Cells activate a DNA damage response (DDR) to maintain genome stability.
  • DDR is typically suppressed during mitosis to prevent errors in chromosome segregation.

Purpose of the Study:

  • To investigate the role of TopBP1 in DNA processing during mitosis.
  • To determine if TopBP1-mediated unscheduled DNA synthesis in mitosis requires translesion synthesis pathways.
  • To understand how DNA damage is managed during cell division.

Main Methods:

  • Utilized genetic analysis in the avian DT40 cell line.
  • Investigated the requirement for Rev1 and PCNA ubiquitylation (K164) in mitotic DNA synthesis.
  • Examined the colocalization of translesion polymerase eta (η) with TopBP1 and FANCD2 during mitosis.

Main Results:

  • TopBP1 stimulates unscheduled DNA synthesis at underreplicated regions during mitosis.
  • This mitotic DNA synthesis does not require the translesion synthesis scaffold factor Rev1.
  • Mitotic DNA synthesis is independent of PCNA ubiquitylation at K164 and translesion polymerase η activity.

Conclusions:

  • TopBP1 plays a crucial role in DNA repair during mitosis by promoting unscheduled DNA synthesis.
  • This TopBP1-dependent process occurs independently of canonical translesion synthesis pathways.
  • The findings highlight a novel mechanism for reducing DNA damage transmission to daughter cells.