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Statements

Subject Item
n2:RIV%2F00064165%3A_____%2F11%3A9959%21RIV12-MZ0-00064165
rdf:type
n8:Vysledek skos:Concept
rdfs:seeAlso
http://dx.doi.org/10.1091/mbc.E10-07-0643
dcterms:description
Nitric 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. Nitric 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.
dcterms:title
NOA1 is an essential GTPase required for mitochondrial protein synthesis NOA1 is an essential GTPase required for mitochondrial protein synthesis
skos:prefLabel
NOA1 is an essential GTPase required for mitochondrial protein synthesis NOA1 is an essential GTPase required for mitochondrial protein synthesis
skos:notation
RIV/00064165:_____/11:9959!RIV12-MZ0-00064165
n8:predkladatel
n9:ico%3A00064165
n3:aktivita
n17:Z n17:P n17:I
n3:aktivity
I, P(1M0520), Z(MSM0021620806)
n3:cisloPeriodika
1
n3:dodaniDat
n10:2012
n3:domaciTvurceVysledku
n4:4688678
n3:druhVysledku
n19:J
n3:duvernostUdaju
n16:S
n3:entitaPredkladatele
n13:predkladatel
n3:idSjednocenehoVysledku
216116
n3:idVysledku
RIV/00064165:_____/11:9959
n3:jazykVysledku
n20:eng
n3:klicovaSlova
NITRIC-OXIDE SYNTHASE; RESPIRATORY-CHAIN; BACILLUS-SUBTILIS; RIBOSOME; DIFFERENTIATION; EXPRESSION; EVOLUTION; APOPTOSIS; DEFECTS; SUBUNIT
n3:klicoveSlovo
n5:SUBUNIT n5:RIBOSOME n5:DEFECTS n5:DIFFERENTIATION n5:EXPRESSION n5:NITRIC-OXIDE%20SYNTHASE n5:EVOLUTION n5:RESPIRATORY-CHAIN n5:APOPTOSIS n5:BACILLUS-SUBTILIS
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[4E5383E1564A]
n3:nazevZdroje
Molecular Biology of the Cell
n3:obor
n14:CE
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
23
n3:projekt
n7:1M0520
n3:rokUplatneniVysledku
n10:2011
n3:svazekPeriodika
22
n3:tvurceVysledku
Kossler, N. Fischer, B. Zemojtel, T. Lightowlers, RN. Mikula, Ivan Chan, D. Nierhaus, K. H. Richter, R. Nijtmans, L. van den Brand, M. Kornak, U. Pech, M. Spoerle, R. Calvaruso, M. A. Vingron, M. Thurisch, B. Mundlos, S. Smeitink, J. Yamamoto, H. Martásek, Pavel Ritz, A. Kolanczyk, M. Schuelke, M.
n3:wos
000285962300001
n3:zamer
n6:MSM0021620806
s:issn
1059-1524
s:numberOfPages
11