ROLE OF TRANSCRIPTION FACTOR ODD-SKIPPED IN AXON MORPHOLOGY

The transcription factor Odd-skipped plays a critical role in the specification of the epidermis, gut, leg and eye in both vertebrates and invertebrates. Although Odd-skipped is well characterized in patterning several tissues, the role in the Drosophila central nervous system remains relatively unexplored. The aim of this study is to examine neuronal morphology when Odd-skipped is miss-expressed ectopically in engrailed neurons or knocked down using RNAi. This study is extensively built on the Gal4/UAS driver system which allows for expression and knockdown in specific neurons. Genetic crosses were performed at both 25°C and 29°C to allow for different expression levels of the transgenes. RNAi lines were subsequently backcrossed to provide two copies of RNAi to further the effects of the knockdown. Both larvae and adult’s central nervous system were dissected, fixed, immuno stained, and imaged. Analysis was performed using ImageJ software. We found that when Odd is expressed in engrailed tissue both axonal tracts and positioning of cell bodies in the tissue changed in both the larvae and adults as compared to respective controls. When Odd is knocked down there are completely random ectopic projections of varying phenotypes in both larvae and adults. Our results suggest that Odd plays a role in regulation of axonal projection patterning in the central nervous system of Drosophila. The relevance of Odd and it’s homologs continues to expand as a regulator of development in several tissues critical to a diverse set of eukaryotic organisms including humans.