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NOA1 is an essential GTPase required for mitochondrial protein synthesis

MPG-Autoren
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Kolanczyk,  Mateusz
Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Pech,  Markus
Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

Zemojte,  Tomasz
Max Planck Society;

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Yamamoto,  Hiroshi
Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society;

Fischer,  Bjoern
Max Planck Society;

Ritz,  Anita
Max Planck Society;

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Kossler,  Nadine
Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society;

Thurisch,  Boris
Max Planck Society;

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Spoerle,  Ralf
Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Kornak,  Uwe
Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Vingron,  Martin
Gene regulation (Martin Vingron), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Nierhaus,  Knud H.
Ribosomes, Max Planck Institute for Molecular Genetics, Max Planck Society;

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Mundlos,  Stefan
Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Zitation

Kolanczyk, M., Pech, M., Zemojte, T., Yamamoto, H., Mikula, I., Calvaruso, M.-A., et al. (2011). NOA1 is an essential GTPase required for mitochondrial protein synthesis. Molecular Biology of the Cell, 22(1), 1-11. doi:10.1091/mbc.E10-07-0643.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0010-77DA-0
Zusammenfassung
NOA1 is an evolutionarily conserved GTP binding protein, which localizes predominantly to mitochondria in mammalian cells. Based on bioinformatic analysis we predicted its possible involvement in ribosomal biogenesis, although, this had not been supported by any experimental evidence. Here we determine NOA1 function through generation of knock-out mice and in-vitro assays. NOA1 deficient mice exhibit mid-gestation lethality associated with a severe developmental defect of the embryo and trophoblast. Primary embryonic fibroblasts isolated from NOA1 knock-out embryos show deficient mitochondrial protein synthesis and a global defect of oxidative phosphorylation (OXPHOS). Additionally, Noa1-/- cells are impaired in staurosporine induced apoptosis. The analysis of mitochondrial ribosomal subunits from Noa1-/- cells by sucrose gradient centrifugation and Western blotting showed anomalous sedimentation, consistent with a defect in mitochondrial ribosome assembly. Further, in vitro experiments revealed that intrinsic NOA1 GTPase activity was stimulated by bacterial ribosomal constituents. Taken together, our data show that NOA1 is required for mitochondrial protein synthesis, likely due to its yet unidentified role in mitoribosomal biogenesis. Thus, NOA1 is required for such basal mitochondrial functions as ATP synthesis and apoptosis.