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Spatial separation between replisome- and template-induced replication stress signaling.

Néstor García-Rodríguez1, Magdalena Morawska1,2, Ronald P Wong1

  • 1Institute of Molecular Biology (IMB), Mainz, Germany.

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|March 28, 2018
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Summary
This summary is machine-generated.

DNA lesions trigger cell cycle checkpoints through daughter-strand gaps processed by Exo1, preventing further DNA damage during S phase. This Rad9-dependent pathway differs from fork-stalling responses.

Keywords:
DNA damage bypassDNA damage checkpointExo1postreplication repairreplication stress

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cellular Biology

Background:

  • Polymerase-blocking DNA lesions are hypothesized to activate checkpoints via single-stranded DNA at stalled replication forks.
  • Re-priming downstream of lesions can create daughter-strand gaps (DSGs) behind replication forks as an alternative to persistent stalling.

Purpose of the Study:

  • To investigate the role of exonuclease 1 (Exo1) in processing DSGs and activating checkpoint responses.
  • To differentiate the checkpoint signaling pathways activated by polymerase-blocking lesions versus other replication stressors.

Main Methods:

  • Utilized genetic analyses in yeast models to study DNA damage response pathways.
  • Investigated the roles of Exo1 and Rad9 in checkpoint activation following DNA damage.
  • Compared checkpoint activation mechanisms under different replication stress conditions.

Main Results:

  • Exo1 processing of DSGs is essential for timely checkpoint activation during S phase.
  • This Exo1-Rad9-dependent pathway is distinct from the Mrc1-dependent response to fork stalling.
  • The primary checkpoint response to polymerase-blocking lesions originates from Exo1-processed DSGs.

Conclusions:

  • Checkpoint signaling in response to polymerase-blocking DNA lesions is primarily mediated by Exo1 processing of postreplicative daughter-strand gaps.
  • This mechanism is distinct from the replication fork-associated checkpoint response, explaining the dichotomy in signaling pathways.