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Global spliceosome activity regulates entry into cellular senescence.

So Mee Kwon1,2, Seongki Min1,3, Un-Woo Jeoun1,3

  • 1Department of Biochemistry, Ajou University School of Medicine, Suwon, Korea.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|December 18, 2020
PubMed
Summary
This summary is machine-generated.

Cellular senescence, a key aging factor, is regulated by spliceosome gene sets before key markers appear. This spliceosome signature may serve as an early senescence indicator.

Keywords:
Sp1oxidative stressreplicative senescencesplicing factorssplicing varianttranscriptome

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Area of Science:

  • Cellular biology
  • Molecular biology
  • Aging research

Background:

  • Cellular senescence is a permanent growth arrest linked to aging, induced by stressors.
  • Alternative splicing is increasingly recognized as a factor in senescence and aging.
  • The precise role of the spliceosome in senescence remains unclear.

Purpose of the Study:

  • To investigate the involvement of spliceosome composition and function in cellular senescence.
  • To identify early molecular markers of senescence.
  • To elucidate the regulatory mechanisms governing the transition to senescence.

Main Methods:

  • Utilized replicative and oxidative stress-induced senescence models in primary human fibroblasts.
  • Analyzed the expression of 58 spliceosomal genes.
  • Investigated the effects of pharmacologic and genetic spliceosome inhibition.
  • Performed transcription factor association analysis, focusing on Sp1.

Main Results:

  • Identified a common shift in 58 spliceosomal gene expression at the pre-senescence stage, preceding senescence-associated β-galactosidase (SA-β-gal) activity.
  • Demonstrated that perturbing spliceosomal genes induces senescence, highlighting the spliceosome's gatekeeper role.
  • Revealed Sp1 as a key regulator, where its depletion suppressed downstream spliceosomal genes and induced senescence.
  • Established that spliceosomal gene sets, not single genes, govern early senescence transition.

Conclusions:

  • Spliceosomal gene sets play a critical role in the early stages of cellular senescence, prior to SA-β-gal expression.
  • A specific spliceosome signature can serve as an early biomarker for senescence.
  • Sp1 is a crucial transcription factor regulating spliceosome-mediated entry into senescence.