Odd-skipped controls neurite morphology and affect cell survival in Drosophila Melanogaster CNS

The transcription factor has been implicated in many developmental processes in . is expressed in a small cluster of neurons (Slater, Levy et al.) in the developing and adult CNS but its role in neurogenesis has so far not been addressed. Here we show that plays a pivotal role in neurite growth and arborization during development. Loss-of- function prevents neurite outgrowth whereas over and miss-expression causes neurite growth and arborization defects. In addition, miss-expression of can induce cell death in some neural sub types. The neurite growth and arborization defects associated with over expression correlates with a reduction in the pre-synaptically targeted protein Bruchpilot in axonal arbours suggesting an overall decrease in Odd neural synapse formation. This is supported by behavioural data showing that larvae in which is overexpressed behave similarly to larvae in which Odd neurons are silenced showing that increasing protein levels affect neural function. Finally, we demonstrate that using RNAi against does not knock down protein but instead cause an increase in protein levels compared to control larvae. This data demonstrates that RNAi can cause up-regulation of protein levels highlighting the importance of verifying protein levels when using RNAi approaches for knock-down.