Autophagy inhibition rescues structural and functional defects caused by the loss of mitochondrial chaperone <i>Hsc70-5</i> in <i>Drosophila</i>.

ABSTRACT: We investigated in larval and adult Drosophila models whether loss of the mitochondrial chaperone Hsc70-5 is sufficient to cause pathological alterations commonly observed in Parkinson disease. At affected larval neuromuscular junctions, no effects on terminal size, bouton size or number, synapse size, or number were observed, suggesting that we studied an early stage of pathogenesis. At this stage, we noted a loss of synaptic vesicle proteins and active zone components, delayed synapse maturation, reduced evoked and spontaneous excitatory junctional potentials, increased synaptic fatigue, and cytoskeleton rearrangements. The adult model displayed ATP depletion, altered body posture, and susceptibility to heat-induced paralysis. Adult phenotypes could be suppressed by knockdo

SUBMITTER: Zhu JY 

PROVIDER: S-EPMC8526020 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature