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Ongoing replication forks delay the nuclear envelope breakdown upon mitotic entry.

Yoshitami Hashimoto1, Hirofumi Tanaka1

  • 1School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, Japan.

The Journal of Biological Chemistry
|November 5, 2020
PubMed
Summary
This summary is machine-generated.

Protecting DNA replication is crucial for cell division. Stalled replication forks can restart in early mitosis before nuclear envelope breakdown, but not efficiently afterward, impacting cell cycle progression.

Keywords:
CDKWee1/Myt1Xenopus egg extractnuclear envelope breakdown (NEB)replication forksreplisome

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Area of Science:

  • Cell Biology
  • Genomics
  • Molecular Biology

Background:

  • DNA replication is vital for genomic stability and cell division.
  • Replication fork stalling can occur due to stress agents, with potential for restart.
  • Failure to restart stalled forks before mitosis leads to replisome disassembly and DNA repair.

Purpose of the Study:

  • To investigate the consequences of simultaneous stalled replication fork release and mitosis induction.
  • To determine the conditions under which stalled forks can restart during mitosis.
  • To understand the relationship between ongoing replication, mitosis timing, and regulatory kinases.

Main Methods:

  • Utilized Xenopus egg extracts for in vitro studies.
  • Induced replication fork stalling using Ara-cytidine-5'-triphosphate.
  • Monitored replication restart, replisome disassembly, nuclear envelope breakdown (NEB), and kinase activity.

Main Results:

  • Stalled forks could restart in early mitosis before NEB with dCTP addition.
  • Restart efficiency decreased significantly after NEB.
  • Replisome disassembly occurred in a p97-dependent manner regardless of restart.
  • Ongoing replication, not stalled forks, delayed NEB in a Wee1/Myt1 kinase-dependent manner.

Conclusions:

  • DNA replication and mitosis are sequentially regulated processes.
  • Ongoing DNA replication directly influences Wee1/Myt1 kinases, modulating cyclin-dependent kinase activity.
  • This regulation ensures the mutually exclusive and sequential occurrence of DNA replication and mitosis.