RBM-5 modulates U2AF large subunit-dependent alternative splicing in C. elegans

Chuanman Zhou, Xiaoyang Gao, Surong Hu, Wenjing Gan, Jing Xu, Yongchao C. Ma, Long Ma*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

A key step in pre-mRNA splicing is the recognition of 3ʹ splicing sites by the U2AF large and small subunits, a process regulated by numerous trans-acting splicing factors. How these trans-acting factors interact with U2AF in vivo is unclear. From a screen for suppressors of the temperature-sensitive (ts) lethality of the C. elegans U2AF large subunit gene uaf-1(n4588) mutants, we identified mutations in the RNA binding motif gene rbm-5, a homolog of the tumor suppressor gene RBM5. rbm-5 mutations can suppress uaf-1(n4588) ts-lethality by loss of function and neuronal expression of rbm-5 was sufficient to rescue the suppression. Transcriptome analyses indicate that uaf-1(n4588) affected the expression of numerous genes and rbm-5 mutations can partially reverse the abnormal gene expression to levels similar to that of wild type. Though rbm-5 mutations did not obviously affect alternative splicing per se, they can suppress or enhance, in a gene-specific manner, the altered splicing of genes in uaf-1(n4588) mutants. Specifically, the recognition of a weak 3ʹ splice site was more susceptible to the effect of rbm-5. Our findings provide novel in vivo evidence that RBM-5 can modulate UAF-1-dependent RNA splicing and suggest that RBM5 might interact with U2AF large subunit to affect tumor formation.

Original languageEnglish (US)
Pages (from-to)1295-1308
Number of pages14
JournalRNA biology
Volume15
Issue number10
DOIs
StatePublished - Oct 3 2018

Keywords

  • 3ʹ splice site
  • RBM5
  • RNA splicing
  • U2AF
  • transcriptome

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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