This study investigates the role of parkin in mitochondrial dysfunction and apoptotic muscle degeneration in Drosophila. Parkin is a ubiquitin-protein ligase involved in the pathogenesis of Parkinson's disease (PD), particularly in autosomal recessive juvenile parkinsonism (AR-JP). Researchers created a Drosophila model of AR-JP by inactivating the parkin gene, leading to reduced lifespan, locomotor defects, and male sterility. The locomotor defects were attributed to apoptotic cell death in muscle subsets, while male sterility resulted from a defect in spermatogenesis. Mitochondrial pathology was identified as an early manifestation of muscle degeneration and a prominent feature of spermatid individualization in parkin mutants. These findings suggest that mitochondrial dysfunction underlies the tissue-specific phenotypes observed in Drosophila parkin mutants and may contribute to the selective cell loss in AR-JP. Parkin is a conserved gene that encodes a protein with an N-terminal ubiquitin-like domain, two carboxy-terminal ring-finger motifs, and an in-between ring-finger (IBR) domain. It functions as an E3 ubiquitin protein ligase, which is involved in the ubiquitination pathway. Loss-of-function mutations in parkin result in an early-onset form of PD known as AR-JP. AR-JP patients display clinical features similar to idiopathic PD, but most cases lack Lewy body pathology, suggesting that Parkin may be required for Lewy body formation or that dopaminergic neuron loss in idiopathic PD and AR-JP may proceed through distinct mechanisms. The study used a mutational approach to inactivate a Drosophila parkin ortholog, leading to viable but short-lived flies with reduced longevity, male sterility, and locomotor defects. These phenotypes were attributed to mitochondrial dysfunction and apoptosis. The results indicate that mitochondrial dysfunction and apoptosis may underlie dopaminergic neuron loss in AR-JP. Furthermore, these findings suggest a mechanistic link between AR-JP and idiopathic PD. The study also examined the role of parkin in the brain, revealing no significant neuronal loss or dopaminergic neuron loss in parkin mutants, although there was a reduction in the size of the cell body and decreased tyrosine hydroxylase immunostaining in the dorsomedial dopaminergic cell cluster. These findings suggest that parkin function is required in the musculature for normal wing posture, flight, and locomotion. The study provides evidence that mitochondrial dysfunction is an early indicator of muscle dysfunction and that muscle pathology is degenerative in nature. The results suggest that mitochondrial pathology and apoptosis are prominent features of IFM degeneration and may underlie dopaminergic neuron loss in AR-JP.This study investigates the role of parkin in mitochondrial dysfunction and apoptotic muscle degeneration in Drosophila. Parkin is a ubiquitin-protein ligase involved in the pathogenesis of Parkinson's disease (PD), particularly in autosomal recessive juvenile parkinsonism (AR-JP). Researchers created a Drosophila model of AR-JP by inactivating the parkin gene, leading to reduced lifespan, locomotor defects, and male sterility. The locomotor defects were attributed to apoptotic cell death in muscle subsets, while male sterility resulted from a defect in spermatogenesis. Mitochondrial pathology was identified as an early manifestation of muscle degeneration and a prominent feature of spermatid individualization in parkin mutants. These findings suggest that mitochondrial dysfunction underlies the tissue-specific phenotypes observed in Drosophila parkin mutants and may contribute to the selective cell loss in AR-JP. Parkin is a conserved gene that encodes a protein with an N-terminal ubiquitin-like domain, two carboxy-terminal ring-finger motifs, and an in-between ring-finger (IBR) domain. It functions as an E3 ubiquitin protein ligase, which is involved in the ubiquitination pathway. Loss-of-function mutations in parkin result in an early-onset form of PD known as AR-JP. AR-JP patients display clinical features similar to idiopathic PD, but most cases lack Lewy body pathology, suggesting that Parkin may be required for Lewy body formation or that dopaminergic neuron loss in idiopathic PD and AR-JP may proceed through distinct mechanisms. The study used a mutational approach to inactivate a Drosophila parkin ortholog, leading to viable but short-lived flies with reduced longevity, male sterility, and locomotor defects. These phenotypes were attributed to mitochondrial dysfunction and apoptosis. The results indicate that mitochondrial dysfunction and apoptosis may underlie dopaminergic neuron loss in AR-JP. Furthermore, these findings suggest a mechanistic link between AR-JP and idiopathic PD. The study also examined the role of parkin in the brain, revealing no significant neuronal loss or dopaminergic neuron loss in parkin mutants, although there was a reduction in the size of the cell body and decreased tyrosine hydroxylase immunostaining in the dorsomedial dopaminergic cell cluster. These findings suggest that parkin function is required in the musculature for normal wing posture, flight, and locomotion. The study provides evidence that mitochondrial dysfunction is an early indicator of muscle dysfunction and that muscle pathology is degenerative in nature. The results suggest that mitochondrial pathology and apoptosis are prominent features of IFM degeneration and may underlie dopaminergic neuron loss in AR-JP.