1. Chromosomes and Gene Expression
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Maturation of selected human mitochondrial tRNAs requires deadenylation

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Cite this article as: eLife 2017;6:e27596 doi: 10.7554/eLife.27596

Abstract

Human mitochondria contain a genome (mtDNA) that encodes essential subunits of the oxidative phosphorylation system. Expression of mtDNA entails multi-step maturation of precursor RNA. In other systems, the RNA life cycle involves surveillance mechanisms, however, the details of RNA quality control have not been extensively characterised in human mitochondria. Using a mitochondrial ribosome profiling and mitochondrial poly(A)-tail RNA sequencing (MPAT-Seq) assay we identify the poly(A)-specific exoribonuclease PDE12 as a major factor for the quality control of mitochondrial non-coding RNAs. The lack of PDE12 results in a spurious polyadenylation of the 3' ends of the mitochondrial (mt-) rRNA and mt-tRNA. While the aberrant adenylation of 16S mt-rRNA did not affect the integrity of the mitoribosome, spurious poly(A) additions to mt-tRNA led to reduced levels of aminoacylated pool of certain mt-tRNAs and mitoribosome stalling at the corresponding codons. Therefore, our data uncover a new, deadenylation-dependent mtRNA maturation pathway in human mitochondria.

Article and author information

Author details

  1. Sarah F Pearce

    MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  2. Joanna Rorbach

    MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  3. Lindsey Van Haute

    MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  4. Aaron R D'Souza

    MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  5. Pedro Rebelo-Guiomar

    MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  6. Christopher A Powell

    MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  7. Ian Brierley

    Department of Pathology, University of Cambridge, Cambridge, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  8. Andrew E Firth

    Department of Pathology, University of Cambridge, Cambridge, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-7986-9520
  9. Michal Minczuk

    MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, United Kingdom
    For correspondence
    mam@mrc-mbu.cam.ac.uk
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-8242-1420

Funding

Medical Research Council (MC_U105697135)

  • Sarah F Pearce
  • Joanna Rorbach
  • Lindsey Van Haute
  • Aaron R D'Souza
  • Pedro Rebelo-Guiomar
  • Christopher A Powell
  • Michal Minczuk

Wellcome (106207)

  • Ian Brierley
  • Andrew E Firth

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Timothy W Nilsen, Case Western Reserve University, United States

Publication history

  1. Received: April 7, 2017
  2. Accepted: July 21, 2017
  3. Accepted Manuscript published: July 26, 2017 (version 1)
  4. Version of Record published: August 4, 2017 (version 2)

Copyright

© 2017, Pearce et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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