The Genetic Control of Fat Body Development and Function in Drosophila melanogaster



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All living organisms struggle to maintain homeostasis. Organisms have evolved various mechanisms to be able to cope with any changes in temperature, pH or nutrient availability. Mammals, for example put a great amount of effort into maintaining glucose homeostasis. Briefly, they achieve regulation of glucose levels in the blood using primarily two hormones that are produced in the pancreas: insulin and glucagon (Bhagavan 2002). Mammals are not only able to maintain glucose levels within the normal range during long periods of fasting, but they also achieve the same outcome when excessive amount of nutrients are introduced through consumption (Bhagavan 2002). When animals fail to achieve homeostasis multiple complications arise. For example, mammals that are not able to maintain glucose at normal levels in the blood stream, due to lack of insulin, suffer from a disease called diabetes. In a similar manner, holometabolous insects like Drosophila melanogaster try to maintain nutrient homeostasis. The name “holometabolous” describes the metamorphosis that these animals undergo. During metamorphosis, dramatic changes take place such as tissue remodeling and apoptosis. However, in order for these changes to happen, it is critical for the animal to be able to manage its energy resources effectively. The fat body, the main organ responsible for energy storage, responds to environmental changes as it tries to maintain homeostasis, which is probably the reason why it is not destroyed during metamorphosis. For the animal to be ready to initiate this process, great amounts of energy need to be stored in the fat body. This is an important step, as during metamorphosis the animal basically starves. Since the intake of energy is impossible, stored energy must be utilized to fuel the various developmental changes. Therefore, given that fat body plays a pivotal role in nutrient circulation and metamorphosis, experiments are needed to further elucidate its involvement in both metamorphosis and nutrient homeostasis. With the first set of experiments I sought to understand if there were any similarities between fat-body remodeling and cancer metastasis. In both processes, cells dissociate and migrate to a different tissue. Thus, I sought to identify if there were any functional similarities between βFTZ-F1, a competence factor that is responsible for the initiation of fat-body remodeling, and its mammalian ortholog, SF-1. With the second set of experiments I sought to understand how insulin signaling is regulated in Drosophila larvae. More specifically, I identified MMP2, a matrix-metalloproteinase to be a possible regulator of the process. Having a better understanding of insulin signaling pathway in Drosophila offers us the possibility to use Drosophila as model organism to study human diseases such as diabetes and high blood pressure.



Insulin signaling, Fat body remodeling, drosophila melanogaster, Matrix-metalloproteinase 2, MMP2, beta ftz-f1, SF-1