Diminution of eIF4E activity suppresses parkin mutant phenotypes (Articolo in rivista)

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Label
  • Diminution of eIF4E activity suppresses parkin mutant phenotypes (Articolo in rivista) (literal)
Anno
  • 2011-01-01T00:00:00+01:00 (literal)
Alternative label
  • Ottone C, Galasso A, Gemei M, Pisa v, Gigliotti S, Piccioni F ,Graziani F, Verrotti di Pianella A (2011)
    Diminution of eIF4E activity suppresses parkin mutant phenotypes
    in Gene (Amst.)
    (literal)
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  • Ottone C, Galasso A, Gemei M, Pisa v, Gigliotti S, Piccioni F ,Graziani F, Verrotti di Pianella A (literal)
Pagina inizio
  • 12 (literal)
Pagina fine
  • 19 (literal)
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  • 470 (literal)
Rivista
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  • PMID: 20869429 (literal)
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  • Pubblicazione (literal)
Note
  • ISI Web of Science (WOS) (literal)
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  • CEINGE-Biotecnologie Avanzate, Via Comunale Margherita 482, 80145 Naples, Italy SEMM-European School of Molecular Medicine, Via Comunale Margherita 482, 80145 Naples, Italy Institute of Genetics and Biophysics “A. Buzzati Traverso”, CNR, Via P. Castellino 111, 80131 Naples, Italy Dipartimento di Biochimica e Biotecnologie Mediche, Via S. Pansini 5, 80131 Naples, Italy (literal)
Titolo
  • Diminution of eIF4E activity suppresses parkin mutant phenotypes (literal)
Abstract
  • Mutations in the human parkin (PARK2) gene cause autosomal recessive-juvenile Parkinson's disease (AR-JP). In Drosophila melanogaster, mutant parkin alleles display a broad range of phenotypic alterations, including female infertility. Here we report that reducing the level of eukaryotic translation initiation factor 4E (eIF4E) activity specifically rescues the female sterile phenotypes associated with the parkinP23 mutant allele. Additional defects, including reduction of pupal viability and body size, are also entirely recovered in both male and female flies of the abovementioned genotype. We further show that a null eIF4E-binding protein (4EBP) allele counteracts the in vivo effects produced, in a parkinP23 mutant background, by the reduction of functional eIF4E copy number. Moreover, Parkin and eIF4E interact in vitro and co-localize at the posterior end of developing oocytes. Finally, we show that eIF4E is over-expressed in parkinP23 mutant ovaries as compared to wild-types. Taken together, our data are consistent with the idea that Parkin and eIF4E act in a common pathway, likely modulating cap-dependent translation initiation events (literal)
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