Literature DB >> 16777843

Nucleolar localization of aprataxin is dependent on interaction with nucleolin and on active ribosomal DNA transcription.

Olivier J Becherel1, Nuri Gueven, Geoff W Birrell, Valérie Schreiber, Amila Suraweera, Burkhard Jakob, Gisela Taucher-Scholz, Martin F Lavin.   

Abstract

The APTX gene, mutated in patients with the neurological disorder ataxia with oculomotor apraxia type 1 (AOA1), encodes a novel protein aprataxin. We describe here, the interaction and interdependence between aprataxin and several nucleolar proteins, including nucleolin, nucleophosmin and upstream binding factor-1 (UBF-1), involved in ribosomal RNA (rRNA) synthesis and cellular stress signalling. Interaction between aprataxin and nucleolin occurred through their respective N-terminal regions. In AOA1 cells lacking aprataxin, the stability of nucleolin was significantly reduced. On the other hand, down-regulation of nucleolin by RNA interference did not affect aprataxin protein levels but abolished its nucleolar localization suggesting that the interaction with nucleolin is involved in its nucleolar targeting. GFP-aprataxin fusion protein co-localized with nucleolin, nucleophosmin and UBF-1 in nucleoli and inhibition of ribosomal DNA transcription altered the distribution of aprataxin in the nucleolus, suggesting that the nature of the nucleolar localization of aprataxin is also dependent on ongoing rRNA synthesis. In vivo rRNA synthesis analysis showed only a minor decrease in AOA1 cells when compared with controls cells. These results demonstrate a cross-dependence between aprataxin and nucleolin in the nucleolus and while aprataxin does not appear to be directly involved in rRNA synthesis its nucleolar localization is dependent on this synthesis.

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Year:  2006        PMID: 16777843     DOI: 10.1093/hmg/ddl149

Source DB:  PubMed          Journal:  Hum Mol Genet        ISSN: 0964-6906            Impact factor:   6.150


  19 in total

Review 1.  Molecular underpinnings of Aprataxin RNA/DNA deadenylase function and dysfunction in neurological disease.

Authors:  Matthew J Schellenberg; Percy P Tumbale; R Scott Williams
Journal:  Prog Biophys Mol Biol       Date:  2015-01-29       Impact factor: 3.667

2.  Lack of aprataxin impairs mitochondrial functions via downregulation of the APE1/NRF1/NRF2 pathway.

Authors:  Beatriz Garcia-Diaz; Emanuele Barca; Andrea Balreira; Luis C Lopez; Saba Tadesse; Sindhu Krishna; Ali Naini; Caterina Mariotti; Barbara Castellotti; Catarina M Quinzii
Journal:  Hum Mol Genet       Date:  2015-05-14       Impact factor: 6.150

Review 3.  DNA repair mechanisms in dividing and non-dividing cells.

Authors:  Teruaki Iyama; David M Wilson
Journal:  DNA Repair (Amst)       Date:  2013-05-16

Review 4.  DNA repair deficiency in neurodegeneration.

Authors:  Dennis Kjølhede Jeppesen; Vilhelm A Bohr; Tinna Stevnsner
Journal:  Prog Neurobiol       Date:  2011-04-30       Impact factor: 11.685

5.  Immunodeficiency, radiosensitivity, and the XCIND syndrome.

Authors:  Richard A Gatti; Elena Boder; Robert A Good
Journal:  Immunol Res       Date:  2007       Impact factor: 2.829

6.  Base excision repair in the mammalian brain: implication for age related neurodegeneration.

Authors:  Peter Sykora; David M Wilson; Vilhelm A Bohr
Journal:  Mech Ageing Dev       Date:  2013-05-02       Impact factor: 5.432

Review 7.  To live or to die: a matter of processing damaged DNA termini in neurons.

Authors:  Sherif F El-Khamisy
Journal:  EMBO Mol Med       Date:  2011-01-19       Impact factor: 12.137

8.  CK2 phosphorylation-dependent interaction between aprataxin and MDC1 in the DNA damage response.

Authors:  Olivier J Becherel; Burkhard Jakob; Amy L Cherry; Nuri Gueven; Markus Fusser; Amanda W Kijas; Cheng Peng; Sachin Katyal; Peter J McKinnon; Junjie Chen; Bernd Epe; Stephen J Smerdon; Gisela Taucher-Scholz; Martin F Lavin
Journal:  Nucleic Acids Res       Date:  2009-12-14       Impact factor: 16.971

Review 9.  Nucleolar activity in neurodegenerative diseases: a missing piece of the puzzle?

Authors:  Rosanna Parlato; Grzegorz Kreiner
Journal:  J Mol Med (Berl)       Date:  2012-11-20       Impact factor: 4.599

10.  Senataxin, defective in ataxia oculomotor apraxia type 2, is involved in the defense against oxidative DNA damage.

Authors:  Amila Suraweera; Olivier J Becherel; Philip Chen; Natalie Rundle; Rick Woods; Jun Nakamura; Magtouf Gatei; Chiara Criscuolo; Alessandro Filla; Luciana Chessa; Markus Fusser; Bernd Epe; Nuri Gueven; Martin F Lavin
Journal:  J Cell Biol       Date:  2007-06-11       Impact factor: 10.539

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