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Progressive degeneration of dopaminergic neurons in the  substantia nigra pars compacta  is the primary cause for motor symptoms observed in Parkinson’s disease (PD). Mutations in leucine-rich repeat kinase 2 ( LRRK2 ) are the most commonly linked contributor to familial PD. LRRK2 is suggested to be involved in a wide variety of cellular processes, but deciphering its role in the pathogenesis of PD has been difficult. Modelling PD in rodents has been a persistent challenge for the field. However, the fruit fly has been exploited to recapitulate PD gene related dopaminergic cell loss. Using the GAL4-UAS system and established models of  hLRRK2  induced eye degeneration in  Drosophila , we conducted an unbiased suppressor/enhancer screen to uncover genetic modifiers of  LRRK2 . We have identified 36 candidate interactors that modify  LRRK2  induced toxicity in the  Drosophila  eye. Importantly, we determined that a subset of these interactors also modified  hLRRK2(I2020T)  induced dopaminergic neuronal loss in the fly brain and uncovered 16 candidates that modify dopaminergic cell loss. Our results suggest LRRK2 may be involved in a wide variety of cellular processes and the results from this screen provide an important genetic resource for further evaluation of LRRK2 function.

LRRK2(I2020T) functional genetic interactors that modify eye degeneration and dopaminergic cell loss in Drosophila