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Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
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RBM-5 modulates U2AF large subunit-dependent alternative splicing in C. elegans.

Chuanman Zhou1, Xiaoyang Gao1, Surong Hu1

  • 1a Center for Medical Genetics, School of Life Sciences , Central South University , Changsha , Hunan , China.

RNA Biology
|October 9, 2018
PubMed
Summary

Mutations in RBM5 suppress defects in RNA splicing caused by U2AF mutations. This suggests RBM5 modulates splicing and may influence tumor formation by interacting with the U2AF large subunit.

Keywords:
3ʹ splice siteRBM5RNA splicingU2AFtranscriptome

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Area of Science:

  • Molecular Biology
  • Genetics
  • RNA Splicing

Background:

  • Pre-mRNA splicing involves recognizing 3' splice sites by U2AF subunits, a process influenced by trans-acting factors.
  • The in vivo interaction between trans-acting factors and U2AF remains largely unknown.

Purpose of the Study:

  • To investigate the in vivo interaction between trans-acting splicing factors and the U2AF large subunit.
  • To identify genes that modulate the function of the U2AF large subunit (UAF-1).

Main Methods:

  • Genetic screen in C. elegans to identify suppressors of uaf-1(n4588) temperature-sensitive lethality.
  • Transcriptome analysis to assess gene expression changes.
  • Functional analysis of identified suppressor mutations in the RBM5 homolog gene (rbm-5).

Main Results:

  • Loss-of-function mutations in rbm-5 suppressed the ts-lethality of uaf-1 mutants.
  • Neuronal expression of rbm-5 rescued the suppression phenotype.
  • rbm-5 mutations partially reversed gene expression abnormalities caused by uaf-1 mutations.
  • rbm-5 mutations modulated alternative splicing in a gene-specific manner, particularly affecting weak 3' splice site recognition.

Conclusions:

  • RBM-5 plays a role in modulating UAF-1-dependent RNA splicing in vivo.
  • RBM5 may interact with the U2AF large subunit, potentially impacting tumor formation.