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Article: NOA1 is an essential GTPase required for mitochondrial protein synthesis

TitleNOA1 is an essential GTPase required for mitochondrial protein synthesis
Authors
Issue Date2011
PublisherAmerican Society for Cell Biology. The Journal's web site is located at http://www.molbiolcell.org/
Citation
Molecular Biology Of The Cell, 2011, v. 22 n. 1, p. 1-11 How to Cite?
AbstractNitric oxide associated-1 (NOA1) is an evolutionarily conserved guanosine triphosphate (GTP) binding protein that localizes predominantly to mitochondria in mammalian cells. On the basis of 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 knockout mice and in vitro assays. NOA1-deficient mice exhibit midgestation lethality associated with a severe developmental defect of the embryo and trophoblast. Primary embryonic fibroblasts isolated from NOA1 knockout 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. Furthermore, 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 adenosine triphosphate (ATP) synthesis and apoptosis. © 2011 Kolanczyk et al.
Persistent Identifierhttp://hdl.handle.net/10722/138951
ISSN
2015 Impact Factor: 4.037
2015 SCImago Journal Rankings: 3.665
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Children's Tumor Fundation, New York2007-01-038
Bundesministerium fur Bildung und ForschungNF1-01GM0844
European CommissionLSHM-CT-2007-037471
German Academic Exchange Service (DAAD, New York)
Alexander-von-Humboldt stipendium
Biotechnology and Biological Sciences Research CouncilBB/F011520/1
Ministry of Education, Youth and Sports1 M 6837805002
0021620806
GAUK252021 102107
German Ministry of Education and Research (BMBF)01GM0862
Funding Information:

We thank Monika Osswald, Petra Schrade, and Carola Dietrich for excellent technical assistance. We also thank Malgorzata Gasperowicz and James Cross for providing template vectors for placenta specific riboprobes. We also acknowledge Laurene Marchand for her contribution in establishing mitochondrial membrane potential assay. M. K. and N. K. were supported by a Young Investigator Award (Grant 2007-01-038) from the Children's Tumor Fundation, New York, and by Bundesministerium fur Bildung und Forschung Grant NF1-01GM0844. This work was also supported by the Sixth Framework of the European Commission, EuroGrow project LSHM-CT-2007-037471. M. P. was supported by a German Academic Exchange Service (DAAD, New York) grant and H. Y. by an Alexander-von-Humboldt stipendium. R.N.L. was supported by grant number BB/F011520/1 from the Biotechnology and Biological Sciences Research Council. I. M. and P. M. are supported by grants 1 M 6837805002 and 0021620806 from the Ministry of Education, Youth and Sports and by grant 252021 102107 from GAUK. M. S. was supported by the Deutsche Forschungsgemeinschaft, Neuro-Cure Exc 257 and is a member of the German network for mitochondrial disorders (mitoNET, 01GM0862), funded by the German Ministry of Education and Research (BMBF).

References

 

DC FieldValueLanguage
dc.contributor.authorKolanczyk, Men_HK
dc.contributor.authorPech, Men_HK
dc.contributor.authorZemojtel, Ten_HK
dc.contributor.authorYamamoto, Hen_HK
dc.contributor.authorMikula, Ien_HK
dc.contributor.authorCalvaruso, MAen_HK
dc.contributor.authorVan Den Brand, Men_HK
dc.contributor.authorRichter, Ren_HK
dc.contributor.authorFischer, Ben_HK
dc.contributor.authorRitz, Aen_HK
dc.contributor.authorKossler, Nen_HK
dc.contributor.authorThurisch, Ben_HK
dc.contributor.authorSpoerle, Ren_HK
dc.contributor.authorSmeitink, Jen_HK
dc.contributor.authorKornak, Uen_HK
dc.contributor.authorChan, Den_HK
dc.contributor.authorVingron, Men_HK
dc.contributor.authorMartasek, Pen_HK
dc.contributor.authorLightowlers, RNen_HK
dc.contributor.authorNijtmans, Len_HK
dc.contributor.authorSchuelke, Men_HK
dc.contributor.authorNierhaus, KHen_HK
dc.contributor.authorMundlos, Sen_HK
dc.date.accessioned2011-09-23T05:43:02Z-
dc.date.available2011-09-23T05:43:02Z-
dc.date.issued2011en_HK
dc.identifier.citationMolecular Biology Of The Cell, 2011, v. 22 n. 1, p. 1-11en_HK
dc.identifier.issn1059-1524en_HK
dc.identifier.urihttp://hdl.handle.net/10722/138951-
dc.description.abstractNitric oxide associated-1 (NOA1) is an evolutionarily conserved guanosine triphosphate (GTP) binding protein that localizes predominantly to mitochondria in mammalian cells. On the basis of 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 knockout mice and in vitro assays. NOA1-deficient mice exhibit midgestation lethality associated with a severe developmental defect of the embryo and trophoblast. Primary embryonic fibroblasts isolated from NOA1 knockout 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. Furthermore, 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 adenosine triphosphate (ATP) synthesis and apoptosis. © 2011 Kolanczyk et al.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Cell Biology. The Journal's web site is located at http://www.molbiolcell.org/en_HK
dc.relation.ispartofMolecular Biology of the Cellen_HK
dc.rightsMolecular Biology of the Cell. Copyright © American Society for Cell Biology.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshAdenosine Triphosphate - biosynthesisen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshEmbryo, Mammalian - abnormalitiesen_HK
dc.subject.meshEmbryonic Developmenten_HK
dc.subject.meshFetal Deathen_HK
dc.subject.meshFibroblastsen_HK
dc.subject.meshGTP Phosphohydrolases - genetics - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIn Situ Hybridizationen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshMitochondria - metabolismen_HK
dc.subject.meshMitochondrial Proteins - biosynthesisen_HK
dc.subject.meshOxidative Phosphorylationen_HK
dc.subject.meshProtein Biosynthesis - geneticsen_HK
dc.subject.meshRNA, Small Interferingen_HK
dc.subject.meshRibosomes - metabolismen_HK
dc.subject.meshStaurosporine - metabolismen_HK
dc.titleNOA1 is an essential GTPase required for mitochondrial protein synthesisen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, D:chand@hkucc.hku.hken_HK
dc.identifier.authorityChan, D=rp00540en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1091/mbc.E10-07-0643en_HK
dc.identifier.pmid21118999-
dc.identifier.pmcidPMC3016967-
dc.identifier.scopuseid_2-s2.0-78651104165en_HK
dc.identifier.hkuros192042en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78651104165&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume22en_HK
dc.identifier.issue1en_HK
dc.identifier.spage1en_HK
dc.identifier.epage11en_HK
dc.identifier.isiWOS:000285962300001-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridKolanczyk, M=11339613300en_HK
dc.identifier.scopusauthoridPech, M=24173748700en_HK
dc.identifier.scopusauthoridZemojtel, T=6603157278en_HK
dc.identifier.scopusauthoridYamamoto, H=36648289100en_HK
dc.identifier.scopusauthoridMikula, I=35199669500en_HK
dc.identifier.scopusauthoridCalvaruso, MA=25647304800en_HK
dc.identifier.scopusauthoridVan Den Brand, M=16040978700en_HK
dc.identifier.scopusauthoridRichter, R=25623367800en_HK
dc.identifier.scopusauthoridFischer, B=26025829700en_HK
dc.identifier.scopusauthoridRitz, A=36341078900en_HK
dc.identifier.scopusauthoridKossler, N=11340017200en_HK
dc.identifier.scopusauthoridThurisch, B=24605642800en_HK
dc.identifier.scopusauthoridSpoerle, R=46961535300en_HK
dc.identifier.scopusauthoridSmeitink, J=35420863000en_HK
dc.identifier.scopusauthoridKornak, U=6602927954en_HK
dc.identifier.scopusauthoridChan, D=7402216545en_HK
dc.identifier.scopusauthoridVingron, M=34574254700en_HK
dc.identifier.scopusauthoridMartasek, P=35325177300en_HK
dc.identifier.scopusauthoridLightowlers, RN=35318014600en_HK
dc.identifier.scopusauthoridNijtmans, L=7003399741en_HK
dc.identifier.scopusauthoridSchuelke, M=6701679466en_HK
dc.identifier.scopusauthoridNierhaus, KH=7103367884en_HK
dc.identifier.scopusauthoridMundlos, S=7005248176en_HK

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