Dysfunction of Mitochondrial Dynamics Induces Endocytosis Defect and Cell Damage in Drosophila Nephrocytes

• Published in: Cells (Basel, Switzerland) Switzerland), 2024-08, Vol.13 (15), p.1253
• Main Authors: Zhu, Jun-Yi, Duan, Jianli, van de Leemput, Joyce, Han, Zhe
• Format: Article
• Language: English
• Subjects: Animals; Antibodies; Cell fusion; Drosophila; Drosophila melanogaster - metabolism; Drosophila Proteins - genetics; Drosophila Proteins - metabolism; Endocytosis; Females; Glomerulus; Insects; Kidneys; Kinases; Laboratories; Marf (MFN); Microscopy; Mitochondria; Mitochondria - metabolism; Mitochondria - pathology; Mitochondrial Dynamics; Organelles; Parkin; Pink1; Podocytes - metabolism; Podocytes - pathology; Protein interaction; Protein Serine-Threonine Kinases - metabolism; Proteins; PTEN-induced putative kinase; Quality control; reactive oxygen species (ROS); Scientific equipment and supplies industry; Software; Structure-function relationships; Ubiquitin-Protein Ligases
• ISSN: 2073-4409; 2073-4409
• DOI: 10.3390/cells13151253

Mitochondria are crucial for cellular ATP production. They are highly dynamic organelles, whose morphology and function are controlled through mitochondrial fusion and fission. The specific roles of mitochondria in podocytes, the highly specialized cells of the kidney glomerulus, remain less understood. Given the significant structural, functional, and molecular similarities between mammalian podocytes and nephrocytes, we employed fly nephrocytes to explore the roles of mitochondria in cellular function. Our study revealed that alterations in the Pink1-Park (mammalian PINK1-PRKN) pathway can disrupt mitochondrial dynamics in nephrocytes. This disruption led to either fragmented or enlarged mitochondria, both of which impaired mitochondrial function. The mitochondrial dysfunction subsequently triggered defective intracellular endocytosis, protein aggregation, and cellular damage. These findings underscore the critical roles of mitochondria in nephrocyte functionality.