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  NOA1 is an essential GTPase required for mitochondrial protein synthesis

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.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-77DA-0 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-77DB-E
Genre: Journal Article
Alternative Title : Mol Biol Cell

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 Creators:
Kolanczyk, Mateusz1, Author              
Pech, Markus2, Author              
Zemojte, Tomasz3, Author
Yamamoto, Hiroshi4, Author              
Mikula, Ivan, Author
Calvaruso, Maria-Antonietta, Author
van den Brand, Mariel, Author
Richter, Ricarda, Author
Fischer, Bjoern3, Author
Ritz, Anita3, Author
Kossler, Nadine1, Author              
Thurisch, Boris3, Author
Spoerle, Ralf1, Author              
Smeitink, Jan, Author
Kornak, Uwe1, Author              
Chan, Danny, Author
Vingron, Martin5, Author              
Martasek, Pavel, Author
Lightowlers, Robert N., Author
Nijtmans, Leo, Author
Schuelke, Markus, AuthorNierhaus, Knud H.6, Author              Mundlos, Stefan1, Author               more..
Affiliations:
1Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433557              
2Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433547              
3Max Planck Society, ou_persistent13              
4Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433549              
5Gene regulation (Martin Vingron), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479639              
6Ribosomes, Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433558              

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 Abstract: 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.

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Language(s): eng - English
 Dates: 2011-01-01
 Publication Status: Published in print
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Title: Molecular Biology of the Cell
  Alternative Title : Mol Biol Cell
Source Genre: Journal
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Pages: - Volume / Issue: 22 (1) Sequence Number: - Start / End Page: 1 - 11 Identifier: ISSN: 1059-1524