Abstract
In holometabolous insects, the steroid hormone 20-hydroxyecdysone (20E), in coordination with juvenile hormone, regulates the major developmental events that promote larval development and the transition from the larval to the pupal stage. Intimately entwined with the hormonal control of development is the control of larval growth and the acquisition of energy stores necessary for the development of the non-feeding pupa and immature adult. Studies of the coordination of insect development and growth have suggested that the larval fat body plays a central role in monitoring animal size and nutritional status by integrating 20E signaling with the insulin signaling pathway. Previous studies have shown that tissue-specific loss of 20E signaling in the fat body causes pupal lethality (Cherbas et al., 2003). Because the fat body is the major organ responsible for nutrient homeostasis, we hypothesized that the observed pupal mortality is due to a metabolic defect. In this paper we show that disruption of 20E signaling in the fat body does not disrupt nutrient storage, animal size at pupariation, or nutrient utilization. We conclude that 20E signaling in the fat body is not necessary for normal pupal metabolism.
