摘要
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 parkin(P23) 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 (4E-BP) allele counteracts the in vivo effects produced in a parkin(P23) 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 parkin(P23) mutant ovaries as compared to wild-types Ta
- 出版日期2011-1-1