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Mutations in  PINK1  and  Parkin/PRKN  cause the degeneration of dopaminergic neurons in familial forms of Parkinson’s disease but the precise pathogenic mechanisms are unknown. The PINK1/Parkin pathway has been described to play a central role in mitochondrial homeostasis by signalling the targeted destruction of damaged mitochondria, however, how disrupting this process leads to neuronal death was unclear until recently. An elegant study in mice revealed that the loss of  Pink1  or  Prkn  coupled with an additional mitochondrial stress resulted in the aberrant activation of the innate immune signalling, mediated via the cGAS/STING pathway, causing degeneration of dopaminergic neurons and motor impairment. Genetic knockout of  Sting  was sufficient to completely prevent neurodegeneration and accompanying motor deficits. To determine whether Sting plays a conserved role in  Pink1/parkin  related pathology, we tested for genetic interactions between  Sting  and  Pink1/parkin  in  Drosophila . Surprisingly, we found that loss of  Sting , or its downstream effector  Relish , was insufficient to suppress the behavioural deficits or mitochondria disruption in the  Pink1/parkin  mutants. Thus, we conclude that phenotypes associated with loss of  Pink1/parkin  are not universally due to aberrant activation of the STING pathway.

The STING pathway does not contribute to behavioural or mitochondrial phenotypes in Drosophila Pink1/parkin or mtDNA mutator models