Format

Send to

Choose Destination
See comment in PubMed Commons below
Trends Genet. 2014 Jul;30(7):298-307. doi: 10.1016/j.tig.2014.05.003. Epub 2014 Jun 12.

Eri1: a conserved enzyme at the crossroads of multiple RNA-processing pathways.

Author information

  • 1Department of Microbiology & Immunology, University of California San Francisco, San Francisco, CA 94143, USA; Sandler Asthma Basic Research Center, University of California San Francisco, San Francisco, CA 94143, USA.
  • 2Department of Cell & Tissue Biology, University of California San Francisco, San Francisco, CA 94143, USA.
  • 3Department of Microbiology & Immunology, University of California San Francisco, San Francisco, CA 94143, USA; Sandler Asthma Basic Research Center, University of California San Francisco, San Francisco, CA 94143, USA. Electronic address: mark.ansel@ucsf.edu.

Abstract

Eri1 is an evolutionarily conserved 3'-5' exoribonuclease that participates in 5.8S rRNA 3' end processing and turnover of replication-dependent histone mRNAs. Over the course of evolution, Eri1 has also been recruited into a variety of conserved and species-specific regulatory small RNA pathways that include endogenous small interfering (si)RNAs and miRNAs. Recent advances in Eri1 biology illustrate the importance of RNA metabolism in epigenetic gene regulation and illuminate common principles and players in RNA biogenesis and turnover. In this review, we highlight Eri1 as a member of a growing class of ribosome- and histone mRNA-associated proteins that have been recruited into divergent RNA metabolic pathways. We summarize recent advances in the understanding of Eri1 function in these pathways and discuss how Eri1 impacts gene expression and physiology in a variety of eukaryotic species. This emerging view highlights the possibility for crosstalk and coregulation of diverse cellular processes regulated by RNA.

KEYWORDS:

RNAi; epigenetic regulation; gene expression; histone mRNA; miRNA; rRNA

PMID:
24929628
PMCID:
PMC4114243
DOI:
10.1016/j.tig.2014.05.003
[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center