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Parkinson's disease ( PD )‐associated Pink1 and Parkin proteins are believed to function in a common pathway controlling mitochondrial clearance and trafficking. Glial cell line‐derived neurotrophic factor ( GDNF ) and its signaling receptor Ret are neuroprotective in toxin‐based animal models of  PD . However, the mechanism by which  GDNF /Ret protects cells from degenerating remains unclear. We investigated whether the  Drosophila  homolog of  Ret  can rescue  Pink1  and  park  mutant phenotypes. We report that a signaling active version of  Ret  ( Ret    MEN2B  ) rescues muscle degeneration, disintegration of mitochondria and  ATP  content of  Pink1  mutants. Interestingly, corresponding phenotypes of  park  mutants were not rescued, suggesting that the phenotypes of  Pink1  and  park  mutants have partially different origins. In human neuroblastoma cells,  GDNF  treatment rescues morphological defects of  PINK 1 knockdown, without inducing mitophagy or Parkin recruitment.  GDNF  also rescues bioenergetic deficits of  PINK  knockdown cells. Furthermore, overexpression of  Ret    MEN2B   significantly improves electron transport chain complex I function in  Pink1  mutant  Drosophila . These results provide a novel mechanism underlying Ret‐mediated cell protection in a situation relevant for human  PD .

Ret rescues mitochondrial morphology and muscle degeneration of Drosophila Pink1 mutants