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Related Experiment Video

Updated: Feb 13, 2026

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SFPQ Promotes Homologous Recombination via mRNA Stabilization of RAD51 and Its Paralogs.

Sofia Gotthold1, Keile R Hansen2, Andrew N Brown2

  • 1Interdisciplinary Program in Quantitative Biosciences, University of California, Santa Barbara, Santa Barbara, CA 93106, USA.

Journal of Molecular Biology
|February 11, 2026
PubMed
Summary

The splicing factor SFPQ stabilizes RAD51 expression to promote DNA repair, independent of direct DNA damage interaction. This reveals indirect RNA-binding protein roles in maintaining genome stability.

Keywords:
DNA double-strand break repair (DSB repair)Homologous recombination (HR)RAD51RAD51 paralogs (RAD51B/RAD51C/RAD51D/XRCC2/XRCC3)SFPQ (PSF)

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • DNA double-strand breaks (DSBs) are repaired via non-homologous end joining (NHEJ) or homologous recombination (HR).
  • Identifying novel factors influencing DSB repair pathways is crucial for understanding genome stability.

Purpose of the Study:

  • To identify non-canonical factors affecting DSB repair outcomes.
  • To elucidate the mechanism by which SFPQ influences DSB repair.

Main Methods:

  • Pooled genetic screens to identify DSB repair factors.
  • Depletion studies to assess SFPQ's role in DSB repair.
  • Analysis of RAD51 and its paralogs' expression and localization.

Main Results:

  • SFPQ depletion alters DSB repair, specifically impacting HR.
  • SFPQ does not localize to DSBs but stabilizes RAD51 and paralog expression.
  • This stabilization occurs independently of p53 activation or DNA damage.

Conclusions:

  • SFPQ contributes to constitutive DSB repair by maintaining RAD51 paralog mRNA stability.
  • SFPQ influences genome stability through indirect mechanisms, not direct DSB interaction.
  • RNA-binding proteins can indirectly modulate genome stability via mRNA regulation.