Fine Tuning of Behavior by RNA Editing

One of the consequences of RNA editing by ADAR enzymes is genetic recoding of messenger RNAs. Of the many examples of this phenomenon, most occur in genes whose products encode proteins involved in fast electrical and chemical neurotransmission. Nowhere is this more apparent than in Drosophila melanogaster , where mutants lacking all ADAR activity display profound neurological phenotypes. We will present evidence that global ADAR mutant phenotypes can be rescued in adult animals by regulated expression of ADAR activities. In addition, we can effectively mimic aspects of the ADAR mutant phenotype by targeted expression of a dominant negative enzyme. These results demonstrate that the presence of edited proteins is necessary for normal adult brain function and that developmental consequences of lacking ADAR function are minimal. We will also show that the lack of edited proteins originating from a single gene results in subtle defects in complex behaviors. A model of the evolution of species‐specific RNA editing for behavioral fine tuning will also be presented.