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

Lookup NU author(s): Dr Hamid Reza Soleimanpour Lichaei, Dr Joao Passos, Dr Mateusz Wydro, Dr Joanna Rorbach, Dr Richard Temperley, Professor Robert Lightowlers, Professor Zofia Chrzanowska-LightowlersORCiD



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. © 2007 Elsevier Inc. All rights reserved.

Publication metadata

Author(s): Soleimanpour-Lichaei HR, Kuhl I, Gaisne M, Passos JF, Wydro M, Rorbach J, Temperley R, Bonnefoy N, Tate W, Lightowlers R, Chrzanowska-Lightowlers Z

Publication type: Article

Publication status: Published

Journal: Molecular Cell

Year: 2007

Volume: 27

Issue: 5

Pages: 745-757

Print publication date: 01/09/2007

ISSN (print): 1097-2765

ISSN (electronic): 1097-4164

Publisher: Cell Press


DOI: 10.1016/j.molcel.2007.06.031


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