Baboon/dSmad2-mediated TGF-beta signaling activates ecdysone receptor-B1 expression during neuronal remodeling in the Drosophila brain. X. Zheng ¹, J. Wang ¹, T.E. Haerry ³, A.Y-H. Wu ¹, J. Martin ³, M.B. O'Connor ³, C-H.J. Lee ², T. Lee ¹. 1) Department of Cell and Structural Biology, University of Illinois, Urbana, IL; 2) Department of Internal Medicine, University of Illinois, Chicago, IL; 3) Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN.

   Metamorphosis of the Drosophila brain involves pruning of many larval-specific dendrites and axons followed by outgrowth of adult-specific processes. From a genetic mosaic screen, we recovered two independent mutations that block neuronal remodeling in the mushroom bodies (MBs). These phenotypically indistinguishable mutations affect Baboon function, a Drosophila TGF-beta/activin type I receptor, and dSmad2, its downstream transcriptional effector. We also show that Punt and Wit, two type II receptors, act redundantly in this process. In addition, we find that overexpression of a dominant negative dActivin interferes with remodeling. Lastly we show that ecdysone receptor EcR-B1 expression is reduced in activin pathway mutants and that restoring EcR-B1 expression significantly rescues remodeling defects. We conclude that the Drosophila Activin signaling pathway mediates neuronal remodeling in part by regulating EcR-B1 expression.