The study investigates the role of the PINK1/Parkin pathway in regulating mitochondrial morphology. Loss-of-function mutations in *PINK1* and *parkin* genes, which encode a serine/threonine kinase and an E3 ubiquitin-protein ligase, respectively, lead to recessive familial Parkinsonism. Genetic studies in *Drosophila* suggest that PINK1 acts upstream of Parkin in a pathway influencing mitochondrial integrity in tissues such as flight muscle and dopaminergic neurons. The authors explore the influence of genetic alterations affecting mitochondrial morphology on *PINK1* and *parkin* mutant phenotypes. They find that heterozygous loss-of-function mutations of *drp1*, which encodes a key mitochondrial fission-promoting component, are lethal in *PINK1* or *parkin* mutant backgrounds. Conversely, increased *drp1* gene dosage and heterozygous loss-of-function mutations affecting mitochondrial fusion-promoting factors OPA1 and Mfn2 strongly suppress the flight muscle degeneration and mitochondrial morphological alterations caused by *PINK1* and *parkin* mutations. Additionally, an eye phenotype associated with increased PINK1/Parkin pathway activity is suppressed by perturbations that reduce mitochondrial fission and enhanced by those that reduce mitochondrial fusion. These findings suggest that the PINK1/Parkin pathway promotes mitochondrial fission and that the loss of mitochondrial and tissue integrity in *PINK1* and *parkin* mutants results from reduced mitochondrial fission.The study investigates the role of the PINK1/Parkin pathway in regulating mitochondrial morphology. Loss-of-function mutations in *PINK1* and *parkin* genes, which encode a serine/threonine kinase and an E3 ubiquitin-protein ligase, respectively, lead to recessive familial Parkinsonism. Genetic studies in *Drosophila* suggest that PINK1 acts upstream of Parkin in a pathway influencing mitochondrial integrity in tissues such as flight muscle and dopaminergic neurons. The authors explore the influence of genetic alterations affecting mitochondrial morphology on *PINK1* and *parkin* mutant phenotypes. They find that heterozygous loss-of-function mutations of *drp1*, which encodes a key mitochondrial fission-promoting component, are lethal in *PINK1* or *parkin* mutant backgrounds. Conversely, increased *drp1* gene dosage and heterozygous loss-of-function mutations affecting mitochondrial fusion-promoting factors OPA1 and Mfn2 strongly suppress the flight muscle degeneration and mitochondrial morphological alterations caused by *PINK1* and *parkin* mutations. Additionally, an eye phenotype associated with increased PINK1/Parkin pathway activity is suppressed by perturbations that reduce mitochondrial fission and enhanced by those that reduce mitochondrial fusion. These findings suggest that the PINK1/Parkin pathway promotes mitochondrial fission and that the loss of mitochondrial and tissue integrity in *PINK1* and *parkin* mutants results from reduced mitochondrial fission.