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The Tgif2 gene contains a retained intron within the coding sequence.

Tiffany A Melhuish1, David Wotton

  • 1Department of Biochemistry and Molecular Genetics, Center for Cell Signaling, University of Virginia, Hospital West, Box 800577, Charlottesville, VA 22908, USA. tam6c@virginia.edu

BMC Molecular Biology
|January 27, 2006
PubMed
Summary

Mouse Tgif2 gene produces two splice variants due to a retained intron, generating functional transcriptional repressors. This alternative splicing is specific to mouse and influenced by intronic sequences.

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Area of Science:

  • Molecular Biology
  • Gene Regulation

Background:

  • TGIF and TGIF2 are homeodomain proteins acting as Smad transcriptional corepressors for TGFbeta signaling.
  • They repress gene expression through interactions with general repressors like mSin3 and DNA binding.

Purpose of the Study:

  • To characterize splice variants of the mouse Tgif2 gene.
  • To investigate the role of a retained intron in Tgif2 gene expression and function.

Main Methods:

  • Polymerase Chain Reaction (PCR) to identify splice variants from mouse cDNA.
  • Reverse Transcription PCR (RT-PCR) to assess intron retention levels.
  • Analysis of protein-protein interactions.

Main Results:

  • Identified two splice variants of mouse Tgif2, one full-length and one with 39 deleted codons.

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  • Mouse Tgif2 mRNA exhibits a retained intron in 25-50% of transcripts, unlike human Tgif2.
  • Both mouse Tgif2 splice variants function as active transcriptional repressors and interact with mSin3.

    • Conclusions:

    • The Tgif2 gene contains a retained intron in the second coding exon, which is differentially spliced in mouse but not human.
    • Alternative splicing is regulated by sequences within the mouse Tgif2 coding region, suggesting an exonic splicing enhancer.
    • Both resulting mouse Tgif2 proteins are functional transcriptional repressors.