SANPODO AND NOTCH ACT IN OPPOSITION TO NUMB TO DISTINGUISH SIBLING NEURON FATES IN THE DROSOPHILA CNS

In Drosophila, most neuronal siblings have different fates ('A/B'). He re we demonstrate that mutations in sanpodo, a tropomodulin actin-bind ing protein homologue, equalize a diverse array of sibling neuron fate s ('B/B'). Loss of Notch signaling gives the same phenotype, whereas l oss of numb gives the opposite phenotype ('A/A'). The identical effect of removing either sanpodo or Notch function on the fates of sibling CNS neurons indicates that sanpodo may act in the Notch signaling path way. In addition, sanpodo and numb show dosage-sensitive interactions and epistasis experiments indicate that sanpodo acts downstream of num b. Taken together, these results show that interactions between sanpod o, the Notch signaling pathway and numb enable CNS sibling neurons to acquire different fates.