The eIF4E-binding protein Eap1p functions in Vts1p-mediated transcript decay

PLoS One. 2012;7(10):e47121. doi: 10.1371/journal.pone.0047121. Epub 2012 Oct 10.

Abstract

Sequence-specific RNA binding proteins can induce the degradation of mRNAs through their ability to recruit proteins that trigger transcript destabilization. For example, Vts1p, the S. cerevisiae member of the Smaug family of RNA binding proteins, is thought to induce transcript decay by recruiting the Ccr4p-Pop2p-Not deadenylase complex to target mRNAs. The resulting deadenylation triggers transcript decapping followed by 5'-to-3' exonucleolytic decay. Here we show that the eIF4E-binding protein, Eap1p, is required for efficient degradation of Vts1p target transcripts and that this role involves the ability of Eap1p to interact with eIF4E. Eap1p does not stimulate deadenylation of Vts1p target transcripts but is instead involved in decapping. Eap1p interacts with Vts1p and mediates an indirect interaction between Vts1p and eIF4E. Taken together these data suggest a model whereby the interaction of Vts1p with Eap1p at target mRNAs stimulates decapping.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Eukaryotic Initiation Factor-4E / metabolism*
  • Protein Binding
  • RNA Caps / metabolism
  • RNA Stability*
  • RNA, Messenger / metabolism
  • RNA-Binding Proteins / genetics
  • RNA-Binding Proteins / metabolism*
  • Saccharomyces cerevisiae Proteins / genetics
  • Saccharomyces cerevisiae Proteins / metabolism*
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*

Substances

  • Eap1 protein, S cerevisiae
  • Eukaryotic Initiation Factor-4E
  • RNA Caps
  • RNA, Messenger
  • RNA-Binding Proteins
  • Saccharomyces cerevisiae Proteins
  • Transcription Factors
  • Vts1 protein, S cerevisiae

Grants and funding

This work was supported by an operating grant from the Canadian Cancer Society. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.