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A G-tract element in apoptotic agents-induced alternative splicing

Yan Hai1, Wenguang Cao, Guodong Liu

  • 1Institute of Medical Biology, Chinese Academy of Medical Sciences & Peking Union Medical College. Kunming, China.

Nucleic Acids Research
|April 29, 2008
PubMed

Insights

Alternative splicing regulates cell fate. A G-tract element (Gt16) mediates apoptotic agent-induced changes in splicing, impacting cell growth and death pathways.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Alternative splicing generates protein diversity from a single pre-mRNA.
  • Dysregulation of alternative splicing is implicated in various diseases.

Purpose of the Study:

  • To investigate the molecular mechanisms by which apoptotic agents regulate alternative splicing.
  • To identify specific sequence elements involved in this regulation.

Main Methods:

  • Targeted mutagenesis to identify critical sequences.
  • Gene transfer assays to assess functional significance.
  • RT-PCR to screen for responsive genes in the human genome.

Main Results:

  • Ro-31-8220 (Ro), an apoptotic agent, decreased the cell growth-promoting Bcl-xL splice variant.
  • A 16-nucleotide G-tract element (Gt16) was identified as critical for this regulation.
  • The Gt16 element conferred Ro-responsiveness to a heterologous gene.
  • Okadaic acid inhibited the Ro-induced splicing changes in a dose-dependent manner.
  • A group of genes containing similar G-tract elements were identified as responsive to Ro and retinoic acid.

Conclusions:

  • The G-tract element (Gt16) is a key regulator of alternative splicing induced by apoptotic agents.
  • This regulatory mechanism impacts genes involved in cell growth and death.
  • The findings suggest a novel pathway for controlling cell fate through alternative splicing.

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