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@ARTICLE{Zhu:137195,
      author       = {Zhu, Jun-Yi and Vereshchagina, Natalia and Sreekumar,
                      Vrinda and Burbulla, Lena F and Costa, Ana C and Daub,
                      Katharina J and Woitalla, Dirk and Martins, L Miguel and
                      Krüger, Rejko and Rasse, Tobias M},
      title        = {{K}nockdown of {H}sc70-5/mortalin induces loss of synaptic
                      mitochondria in a {D}rosophila {P}arkinson's disease model.},
      journal      = {PLOS ONE},
      volume       = {8},
      number       = {12},
      issn         = {1932-6203},
      address      = {San Francisco, California, US},
      publisher    = {PLOS},
      reportid     = {DZNE-2020-03517},
      pages        = {e83714},
      year         = {2013},
      abstract     = {Mortalin is an essential component of the molecular
                      machinery that imports nuclear-encoded proteins into
                      mitochondria, assists in their folding, and protects against
                      damage upon accumulation of dysfunctional, unfolded proteins
                      in aging mitochondria. Mortalin dysfunction associated with
                      Parkinson's disease (PD) increases the vulnerability of
                      cultured cells to proteolytic stress and leads to changes in
                      mitochondrial function and morphology. To date, Drosophila
                      melanogaster has been successfully used to investigate
                      pathogenesis following the loss of several other
                      PD-associated genes. We generated the first
                      loss-of-Hsc70-5/mortalin-function Drosophila model. The
                      reduction of Mortalin expression recapitulates some of the
                      defects observed in the existing Drosophila PD-models, which
                      include reduced ATP levels, abnormal wing posture, shortened
                      life span, and reduced spontaneous locomotor and climbing
                      ability. Dopaminergic neurons seem to be more sensitive to
                      the loss of mortalin than other neuronal sub-types and
                      non-neuronal tissues. The loss of synaptic mitochondria is
                      an early pathological change that might cause later
                      degenerative events. It precedes both behavioral
                      abnormalities and structural changes at the neuromuscular
                      junction (NMJ) of mortalin-knockdown larvae that exhibit
                      increased mitochondrial fragmentation. Autophagy is
                      concomitantly up-regulated, suggesting that mitochondria are
                      degraded via mitophagy. Ex vivo data from human fibroblasts
                      identifies increased mitophagy as an early pathological
                      change that precedes apoptosis. Given the specificity of the
                      observed defects, we are confident that the loss-of-mortalin
                      model presented in this study will be useful for further
                      dissection of the complex network of pathways that underlie
                      the development of mitochondrial parkinsonism.},
      keywords     = {Animals / Autophagy: genetics / Cell Survival: genetics /
                      Disease Models, Animal / Dopaminergic Neurons: metabolism /
                      Drosophila / Female / Gene Knockdown Techniques / Gene
                      Silencing / Genes, Essential / HSP70 Heat-Shock Proteins:
                      genetics / Humans / Mitochondria: genetics / Mitochondria:
                      metabolism / Neurons: metabolism / Parkinson Disease:
                      genetics / Parkinson Disease: metabolism / Phenotype /
                      Synapses: metabolism / HSP70 Heat-Shock Proteins (NLM
                      Chemicals) / mortalin (NLM Chemicals)},
      cin          = {AG Gasser 1},
      ddc          = {610},
      cid          = {I:(DE-2719)1210000},
      pnm          = {345 - Population Studies and Genetics (POF3-345)},
      pid          = {G:(DE-HGF)POF3-345},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24386261},
      pmc          = {pmc:PMC3875477},
      doi          = {10.1371/journal.pone.0083714},
      url          = {https://pub.dzne.de/record/137195},
}