mtRF1a Is a Human Mitochondrial Translation Release Factor Decoding the Major Termination Codons UAA and UAG

Hamid Reza Soleimanpour-Lichaei, Inge Kühl, Mauricette Gaisne, Joao F. Passos, Mateusz Wydro, Joanna Rorbach, Richard Temperley, Nathalie Bonnefoy, Warren Tate, Robert Lightowlers, Zofia Chrzanowska-Lightowlers

Research output: Contribution to journalArticlepeer-review

86 Scopus citations

Abstract

Human mitochondria contain their own genome, encoding 13 polypeptides that are synthesized within the organelle. The molecular processes that govern and facilitate this mitochondrial translation remain unclear. Many key factors have yet to be characterized-for example, those required for translation termination. All other systems have two classes of release factors that either promote codon-specific hydrolysis of peptidyl-tRNA (class I) or lack specificity but stimulate the dissociation of class I factors from the ribosome (class II). One human mitochondrial protein has been previously identified in silico as a putative member of the class I release factors. Although we could not confirm the function of this factor, we report the identification of a different mitochondrial protein, mtRF1a, that is capable in vitro and in vivo of terminating translation at UAA/UAG codons. Further, mtRF1a depletion in HeLa cells led to compromised growth in galactose and increased production of reactive oxygen species.

Original languageEnglish (US)
Pages (from-to)745-757
Number of pages13
JournalMolecular Cell
Volume27
Issue number5
DOIs
StatePublished - Sep 7 2007

Keywords

  • RNA

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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