Parkinson's disease (PD) is a progressive neurodegenerative disorder affecting approximately 1% of the population over the age of 60. Current therapies for PD are incapable of modifying the progression of the disease, however the development of more effective therapies is limited by a lack of understanding of the pathogenesis of PD. Although most cases of PD are sporadic, approximately 10% of cases are inherited due to mutations in at least six different genes, including pinkl, parkin, and LRRK2. An understanding of the endogenous functions of these genes, as well as the mechanisms by which mutations in these genes contribute to the development of PD, would provide significant insight into the pathogenesis of the disease. Furthermore, given the diversity of genetic factors associated with PD, a crucial question is whether different genetic forms of the disease represent distinct molecular etiologies, or whether some or all of these genes function in common pathways. In this work, we demonstrate that the Drosophila pinkl homolog plays a crucial role in maintaining mitochondrial structure and function via regulating mitochondrial fusion/fission dynamics. Interestingly, pinkl mutant phenotypes are highly similar, if not identical, to phenotypes observed in fly parkin mutants, and genetic epistasis experiments indicate that pinkl and parkin function in a common genetic pathway with parkin downstream. In contrast, neither loss- or gain-of-function of the fly LRRK2 homolog (lrrk) affects mitochondrial structure, and epistasis experiments suggest that lrrk functions in a distinct pathway from pinkl/parkin. Rather, lrrk mutants show profound defects in endolysosomal function, including impaired transport of early endosomes, dramatically enlarged lysosomes that abnormally accumulate lipid, and activation of autophagy. Consistent with a role for lrrk in endolysosomal membrane transport, Lrrk localizes to the membranes of endosomes and lysosomes, and physically and genetically interacts with Rab5 and Rab9. Collectively, these data suggest the existence of at least two pathogenic pathways for PD: a pinkl/parkin pathway regulating mitochondrial function, and a LRRK2 pathway regulating endolysosomal membrane transport. Thus, pathway-specific therapies may need to be developed for PD patients of diverse molecular etiologies.