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The human mitochondrial ribosome recycling factor is essential for cell viability

Lookup NU author(s): Dr Joanna Rorbach, Dr Mateusz Wydro, Marcin Pekalski, Professor Robert Lightowlers, Professor Zofia Chrzanowska-LightowlersORCiD

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Abstract

The molecular mechanism of human mitochondrial translation has yet to be fully described. We are particularly interested in understanding the process of translational termination and ribosome recycling in the mitochondrion. Several candidates have been implicated, for which subcellular localization and characterization have not been reported. Here, we show that the putative mitochondrial recycling factor, mtRRF, is indeed a mitochondrial protein. Expression of human mtRRF in fission yeast devoid of endogenous mitochondrial recycling factor suppresses the respiratory phenotype. Further, human mtRRF is able to associate with Escherichia coli ribosomes in vitro and can associate with mitoribosomes in vivo. Depletion of mtRRF in human cell lines is lethal, initially causing profound mitochondrial dysmorphism, aggregation of mitoribosomes, elevated mitochondrial superoxide production and eventual loss of OXPHOS complexes. Finally, mtRRF was shown to co-immunoprecipitate a large number of mitoribosomal proteins attached to other mitochondrial proteins, including putative members of the mitochondrial nucleoid.

Publication metadata

Author(s): Rorbach J, Richter R, Wessels HJ, Wydro M, Pekalski M, Farhoud M, Kuhl I, Gaisne M, Bonnefoy N, Smeitink JA, Lightowlers RN, Chrzanowska-Lightowlers ZMA

Publication type: Article

Publication status: Published

Journal: Nucleic Acids Research

Year: 2008

Volume: 36

Issue: 18

Pages: 5787-5799

Date deposited: 06/04/2010

ISSN (print): 0305-1048

ISSN (electronic): 1362-4962

Publisher: Oxford University Press

URL: http://dx.doi.org/10.1093/nar/gkn576

DOI: 10.1093/nar/gkn576

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