Functional analysis of mitochondrial metabolism in Drosphila oogenesis and embryogenesis

Abstract

Mitochondria synthesizes ATP which is the major source of cellular energy during oxidative phosphorylation in electron transport chain present in inner membrane of mitochondria. Previous studies showed the importance of mitochondrial dynamics and its function during oogenesis in Drosophila melanogaster. In this thesis I have attempted to examine the role of mitochondrial metabolism during embryogenesis and oogenesis. Inhibition of genes involved in mitochondrial metabolism was done using RNAi mediated knockdown with Nanos Gal4 expressed during oogenesis and embryogenesis and c306 Gal4 in follicle cells. RNAi mediated knockdown of subunits of components of complex 1, 3 and 5 of mitochondrial electron transport chain caused lethality in embryos. RNAi mutants of key proteins in these complexes resulted in increased pAMPK caused by a decrease in ATP levels. This caused disruption in actomyosin ring shape during cellularisation and mitochondrial transport across the apicobasal axis in the embryo. Future studies on mitochondrial shape and function change in these mutants along with analysis of the developmental pathways will yield an analysis of steps of Drosophila embryogenesis that will depend on mitochondrial metabolism.