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CELF2 Promotes Tau Exon 10 Inclusion via Hinge Domain-Mediated Nuclear Condensation, Driving Cognitive Dysfunction in

Lizhen Chen1

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Summary

The RNA-binding protein CELF2 promotes tau exon 10 inclusion, crucial for regulating 4R tau. Its condensation capacity, driven by an intrinsically disordered region, is vital for splicing and impacts neurodegeneration.

Keywords:
CELF2NOVA2SFPQTurboIDalternative splicingcondensatehinge domainintrinsically disordered regiontau

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Area of Science:

  • Molecular Biology
  • Neuroscience
  • RNA Splicing

Background:

  • Alternative splicing of the MAPT gene generates 3R and 4R tau isoforms.
  • Disruption of the 4R:3R ratio is a hallmark of tauopathies.
  • Mechanisms controlling tau exon 10 splicing are not fully understood.

Purpose of the Study:

  • Identify key regulators of tau exon 10 splicing.
  • Investigate the role of RNA-binding proteins in tau splicing.
  • Elucidate the molecular mechanisms of tau splicing regulation.

Main Methods:

  • RNA-binding protein CELF2 identification and functional analysis.
  • CRISPR-based imaging to visualize RNA-protein interactions.
  • Proteomic analysis to identify CELF2 interactors.
  • In vivo studies in mouse models.

Main Results:

  • CELF2 promotes tau exon 10 inclusion, maintaining the 4R:3R ratio.
  • An intrinsically disordered region in CELF2 drives condensate formation essential for splicing.
  • CELF2 condensates colocalize with tau RNA, involving NOVA2 and SFPQ.
  • CELF2 condensation capacity correlates with 4R tau expression and affects cognitive function.

Conclusions:

  • CELF2 acts as a key regulator of tau exon 10 splicing through condensate formation.
  • This condensate-based mechanism has implications for tauopathies and neurodegeneration.
  • Targeting CELF2-mediated splicing could offer therapeutic strategies for tauopathies.