The fat body cortical actin network regulates Drosophila inter-organ nutrient trafficking, signaling, and adipocyte cell size

Defective nutrient storage and adipocyte enlargement (hypertrophy) are emerging features of metabolic syndrome and type 2 diabetes. How the cytoskeletal network contributes to nutrient uptake, fat storage, and adipocyte size remains poorly understood. Utilizing the Drosophila larval fat body (FB) as a model adipose tissue, we show that a specific actin isoform—Act5C—forms the cortical actin network necessary for inter-organ lipid trafficking. Act5C also promotes FB tissue expansion during larval development so larvae can store sufficient biomass for metamorphosis. We find FB-specific loss of Act5C, but not other Drosophila actins, perturbs FB triglyceride (TG) storage in lipid droplets (LDs), resulting in developmentally delayed larvae that fail to develop into flies. Act5C localizes to the FB cell surface where it intimately contacts peripheral LDs (pLDs), forming a cortical actin network together with spectrins for cell architectural support. While both the cortical actin and spectrin..., These are datasets associated with cell size quantification.,