This study investigates the role of Parkin, a protein involved in ubiquitination and mitochondrial function, in the pathogenesis of autosomal recessive juvenile parkinsonism (AR-JP). The authors created a Drosophila model of AR-JP by generating null mutants of the *parkin* gene, which encodes Parkin. These mutants exhibit reduced lifespan, locomotor defects, and male sterility. The locomotor defects are due to apoptotic cell death in muscle subsets, while the male sterile phenotype results from a defect in spermatid individualization. Mitochondrial pathology is the earliest manifestation of muscle degeneration and a prominent characteristic of individualizing spermatids in *parkin* mutants. These findings suggest that mitochondrial dysfunction and apoptosis underlie the tissue-specific phenotypes observed in *parkin* mutants and may be a common mechanism in AR-JP and other forms of Parkinson's disease (PD). The study provides insights into the molecular mechanisms of neurodegeneration in PD and highlights the potential link between AR-JP and idiopathic PD.This study investigates the role of Parkin, a protein involved in ubiquitination and mitochondrial function, in the pathogenesis of autosomal recessive juvenile parkinsonism (AR-JP). The authors created a Drosophila model of AR-JP by generating null mutants of the *parkin* gene, which encodes Parkin. These mutants exhibit reduced lifespan, locomotor defects, and male sterility. The locomotor defects are due to apoptotic cell death in muscle subsets, while the male sterile phenotype results from a defect in spermatid individualization. Mitochondrial pathology is the earliest manifestation of muscle degeneration and a prominent characteristic of individualizing spermatids in *parkin* mutants. These findings suggest that mitochondrial dysfunction and apoptosis underlie the tissue-specific phenotypes observed in *parkin* mutants and may be a common mechanism in AR-JP and other forms of Parkinson's disease (PD). The study provides insights into the molecular mechanisms of neurodegeneration in PD and highlights the potential link between AR-JP and idiopathic PD.