A screen for suppressors of unfulfilled reveals novel roles for genes in Drosophila mushroom body development. Karen E. Bates¹, Carl Sung², Joshua Meldon¹, Liam Hilson¹, Steven Robinow¹. 1) University of Hawaii Department of Biology 2450 Campus Road Honolulu, HI 96822; 2) University of Chaminade Department of Natural Sciences and Mathematics Honolulu, HI 96822.

   The Drosophila mushroom body (MB) is an organized collection of interneurons that is required for learning and memory. Over 200 genes are known to be expressed in the MB, yet the genetic hierarchies that control MB development are relatively unknown. Given the sequential birth order and the unique patterning of , '/', and / neuron projections, it is likely that specific gene cascades are required for the different guidance events that form the characteristic lobes of the MB. Previously, we have shown that the nuclear receptor UNFULFILLED (UNF), a transcription factor, is required for the differentiation of all MB neurons. However, the requirement of unf differs among the three subtypes of MB neurons. These subtype-specific regulatory roles further emphasize the need to identify interacting genes in the MB. We have developed and utilized a classical genetic suppressor screen, which takes advantage of the fact that ectopic expression of unf causes lethality, to identify candidate genes that act downstream of UNF. We hypothesized that reducing the copy number of unf-target genes will suppress the unf-induced lethality. We have identified 22 genomic regions on chromosome 3 that may encode unf-interacting genes. To test whether candidate genes in these regions impact MB development, we performed a secondary screen in which the morphologies of the MBs of doubly heterozygous animals were examined. To date, defects were observed in four genes found within four different genomic regions of seven regions that were tested, ;unf/+;failed axon connections/+, ;unf/+;axin/+, ;unf/+;dopamine R2/+, and ;unf/+;tailless/+ flies. These results document a previously undescribed role for tailless, an unexpected morphological defect for dopamine R2, and has identified two genes, failed axon connections and axin, that were not previously known to be expressed in the MB.