Cryptic intron activation within the large exon of the mouse polymeric immunoglobulin receptor gene: cryptic splice

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An Integrated Approach for Microprotein Identification and Sequence Analysis
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An Integrated Approach for Microprotein Identification and Sequence Analysis

Published on: July 12, 2022

S R Bruce1, C S Kaetzel, M L Peterson

  • 1Department of Microbiology, University of Kentucky College of Medicine, Lexington, KY 40536, USA.

Nucleic Acids Research
|August 14, 1999
PubMed

Insights

Deleting a small sequence in the mouse polymeric immuno-globulin receptor (pIgR) gene exon activated cryptic splice sites. This suggests the splicing machinery co-recognizes these sites, influencing gene expression.

Area of Science:

  • Molecular Biology
  • Genetics
  • RNA Splicing

Background:

  • The fourth exon of the mouse polymeric immuno-globulin receptor (pIgR) gene is constitutively spliced.
  • This exon encodes two immunoglobulin-like extracellular protein domains.

Purpose of the Study:

  • To investigate the impact of deleting a specific sequence within the pIgR fourth exon on alternative splicing.
  • To determine the role of cryptic splice sites in regulating pIgR gene expression.

Main Methods:

  • Deletion mutagenesis of the mouse pIgR fourth exon.
  • Analysis of mRNA splicing patterns using sequencing.
  • Site-directed mutagenesis of cryptic splice sites.

Main Results:

  • Deletion of an 84 nt sequence activated both cryptic 5' and 3' splice sites flanking a 78 nt intron.
  • Activation of the cryptic 3' splice site was likely due to creating a better splice site sequence.
  • Point mutations inactivating cryptic splice sites abolished the cryptic splicing event, indicating co-recognition.

Conclusions:

  • Cryptic splice sites within the pIgR fourth exon can be activated by specific sequence deletions.
  • The splicing machinery appears to co-recognize the activated cryptic 5' and 3' splice sites.
  • This finding provides insights into the regulation of gene expression and alternative splicing mechanisms.

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