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SFPQ helps prevent repeat-element genome instability

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Research area:biology-genetics

What the study found

The study found that SFPQ, an RNA-binding protein, helps suppress genome instability linked to R-loops, which are three-stranded nucleic acid structures made of an RNA:DNA hybrid and displaced single-stranded DNA. The effect was reported at repetitive DNA regions such as telomeres, pericentromeres, LINE-1, and SINE elements.

Why the authors say this matters

The authors say this matters because persistent R-loops can drive conflicts with transcription and replication, and repeat-rich parts of the human genome are prone to R-loop formation. The findings indicate that SFPQ helps maintain genome stability in these regions and are reported to correlate with improved survival of sarcoma patients.

What the researchers tested

The researchers examined whether SFPQ binds R-loops, associates with chromatin containing R-loops, and recruits the histone H3.3-specific chaperone DAXX. They also tested what happens when SFPQ is lost, including effects on histone H3.3 incorporation, replication stress, DNA damage, cytoplasmic DNA, and cGAS/STING innate immune signaling.

What worked and what didn't

SFPQ showed in-vitro R-loop binding activity and was associated with chromatin containing R-loops. The study reports that SFPQ recruits DAXX to repeat elements to preserve a correct nucleosome template, which counteracts R-loop accumulation; when SFPQ was lost, DAXX was displaced, histone H3.3 incorporation was reduced, and replication stress-mediated genome instability increased. Loss of SFPQ also led to cytoplasmic DNA and activation of cGAS/STING signaling.

What to keep in mind

The abstract does not describe detailed experimental design, sample sizes, or study limitations. The survival finding is stated as a correlation in sarcoma patients, so the abstract does not show that SFPQ caused the survival difference.

Key points

  • SFPQ suppresses R-loop–mediated replication stress and DNA damage at repeat DNA elements.
  • SFPQ binds R-loops in vitro and associates with chromatin containing R-loops.
  • SFPQ recruits DAXX, the histone H3.3-specific chaperone, to help maintain nucleosome structure.
  • Loss of SFPQ reduces histone H3.3 incorporation and increases genome instability.
  • Loss of SFPQ also activates cGAS/STING innate immune signaling and is reported to correlate with improved sarcoma survival.

Disclosure

Research title:
SFPQ helps prevent repeat-element genome instability
Authors:
Alessandro Ferrando, Michele Giaquinto, Luisa M. R. Napolitano, Giulia Canarutto, Alessandro Framarini, Alice Gambelli, Pamela Veneziano Broccia, Annie Zappone, Eleonora Petti, Chiara Boncristiani, Andrea Parlante, Silvia Onesti, Silvano Piazza, Roberta Benetti, Stefan Schoeftner
Institutions:
Centro Nacional de Análisis Genómico, Elettra-Sincrotrone Trieste S.C.p.A., Elettra-Sincrotrone Trieste S.C.p.A., International Centre for Genetic Engineering and Biotechnology, International Centre for Genetic Engineering and Biotechnology, International Centre for Genetic Engineering and Biotechnology, National Cancer Institute, University of Trieste, University of Trieste, University of Trieste, University of Trieste, University of Trieste, University of Trieste, University of Trieste, University of Trieste, University of Trieste, University of Trieste, University of Trieste, University of Trieste, University of Turin, University of Udine
Publication date:
2026-02-24
DOI:
10.1038/s41467-026-69479-w
OpenAlex record:
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AI provenance: This post was generated by gpt-5.4-mini (OpenAI). The original authors did not write or review this post.

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