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Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase
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XRCC2 Regulates Replication Fork Progression during dNTP Alterations.

Sneha Saxena1, Kumar Somyajit1, Ganesh Nagaraju1

  • 1Department of Biochemistry, Indian Institute of Science, Bangalore 560012, India.

Cell Reports
|December 20, 2018
PubMed
Summary
This summary is machine-generated.

RAD51 paralogs XRCC2 and RAD51D control DNA synthesis during nucleotide pool changes. Their absence causes replication stress and DNA damage, highlighting their role in genome stability.

Keywords:
ATR signalingRAD51 paralogsdNTP poolsfork slowinggenome stabilityreplication stressribonucleotide reductase

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Area of Science:

  • Genetics
  • Molecular Biology
  • DNA Repair

Background:

  • RAD51 paralogs are crucial for genomic integrity.
  • They protect stalled replication forks and facilitate homology-directed repair (HDR) of double-strand breaks.

Purpose of the Study:

  • To investigate the role of RAD51 paralogs, specifically XRCC2 and RAD51D, in DNA synthesis regulation during nucleotide pool alterations.
  • To elucidate the mechanism by which XRCC2 controls replication fork progression independently of HDR.

Main Methods:

  • Investigated XRCC2 and RAD51D function during dinucleotide triphosphate (dNTP) alterations.
  • Assessed RRM2 levels and nucleotide pools in XRCC2-deficient cells.
  • Examined the role of ATR signaling and XRCC2 phosphorylation (Ser247).

Main Results:

  • XRCC2 and RAD51D restrain DNA synthesis during dNTP pool alterations, independent of HDR.
  • XRCC2 absence leads to elevated RRM2, increased nucleotide pools, unrestrained fork progression, and DNA damage.
  • This function is regulated by ATR signaling via XRCC2 phosphorylation at Ser247.

Conclusions:

  • RAD51 paralogs XRCC2 and RAD51D play a novel role in controlling replication fork progression during nucleotide pool imbalances.
  • These findings reveal a mechanism for maintaining genome stability under conditions of altered dNTP availability.