I received my PhD from the University of Edinburgh where I worked with Ilan Davis to study mRNA localization and RNA-binding proteins that regulate development and synaptic plasticity in Drosophila. We identified the uncharacterized Drosophila ortholog of mammalian Syncrip (Syp), which is a component of trafficked neuronal ribonucleoprotein (RNP) complexes and showed that it is required for proper mRNA transport and translational control in the oocyte and embryo. We also explored Syp function in the Drosophila nervous system and showed that it regulates synaptic growth and expression of mRNAs encoding key synaptic proteins at the larval neuromuscular junction. I then pursued postdoctoral training and a subsequent research scientist position with Ken Stuart at the Center for Global Infectious Disease Research in Seattle. Here, I investigate mitochondrial mRNA editing in the protozoan parasite Trypanosoma brucei. T. brucei and related T. cruzi and Leishmania species cause Human African Trypanosomiasis, Chagas’ disease, and Leishmaniases respectively, resulting in serious global health and economic consequences. New drugs are needed to treat these pathogens because existing therapeutics are antiquated, have severe side effects, and resistance is developing. Kinetoplastid parasites rely upon mitochondrial mRNA editing, which is a unique form of mRNA maturation, to generate translatable mRNAs encoding essential mitochondrial respiratory chain and ribosomal subunits. Because editing is essential to the parasites but absent from human and animal hosts, it is an attractive target for new drugs. I use a variety of techniques including RNA-CLIP, deep mutational scanning, cross-linking/mass spectrometry, and integrative modeling to study the physical and functional interactions between proteins and RNAs within the essential complexes responsible for RNA editing in kinetoplastid pathogens.