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PLK1 regulates the PrimPol damage tolerance pathway during the cell cycle.

Laura J Bailey1, Rebecca Teague1, Peter Kolesar1

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Science Advances
|December 3, 2021
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Summary

Polo-like kinase 1 (PLK1) regulates Primase-Polymerase (PrimPol) through phosphorylation, preventing genomic instability. Dysregulation of this process leads to DNA damage and reduced cell survival during replication stress.

Keywords:
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Area of Science:

  • Molecular Biology
  • Cell Cycle Regulation
  • DNA Replication and Repair

Background:

  • Replication stress and DNA damage can stall DNA replication forks, hindering genome synthesis.
  • Damage tolerance pathways, including repriming by Primase-Polymerase (PrimPol), are crucial for bypassing DNA lesions during S phase.
  • The regulatory mechanisms governing PrimPol activity remain largely unelucidated.

Purpose of the Study:

  • To investigate the regulatory mechanisms controlling Primase-Polymerase (PrimPol) function.
  • To determine the role of Polo-like kinase 1 (PLK1) in PrimPol regulation.
  • To assess the consequences of dysregulated PrimPol activity on genomic stability.

Main Methods:

  • Investigated the phosphorylation of PrimPol by Polo-like kinase 1 (PLK1) at a conserved residue.
  • Analyzed cell cycle-dependent phosphorylation patterns of PrimPol.
  • Assessed the impact of PLK1 inhibition on PrimPol recruitment, replication stress response, and genomic integrity using various genotoxic treatments.

Main Results:

  • Demonstrated that PLK1 phosphorylates PrimPol at a key residue, modulating its chromatin recruitment throughout the cell cycle.
  • Showed that this phosphorylation is dynamically regulated in response to replication stress.
  • Found that loss of PLK1-dependent PrimPol regulation results in chromosome breaks, micronuclei formation, and decreased cell survival following exposure to camptothecin, olaparib, and UV-C radiation.

Conclusions:

  • PLK1-mediated phosphorylation is a critical regulator of PrimPol activity, ensuring proper repriming during DNA replication stress.
  • Aberrant repriming due to loss of PLK1 regulation leads to significant genomic instability.
  • These findings underscore the importance of precise regulation of DNA damage tolerance pathways for maintaining genome integrity.