Sanpodo and Notch act in opposition to Numb to distinguish sibling neuron fates in the Drosophila CNS

• DOI: 10.1242/dev.125.10.1857
• Publication Date: 2021-04-26T04:09:09Z
• Authors: James B. Skeath; Chris Q. Doe
• Keywords: Central Nervous System; Neurons; 0301 basic medicine; Receptors, Notch; Microfilament Proteins; Membrane Proteins; Nuclear Proteins; Epistasis, Genetic; Genes, Insect; Juvenile Hormones; 03 medical and health sciences; Phenotype; Mutagenesis; Mutation; Animals; Drosophila Proteins; Insect Proteins; Cell Lineage; Drosophila; Carrier Proteins; Signal Transduction

ABSTRACT In Drosophila, most neuronal siblings have different fates (‘A/B’). Here we demonstrate that mutations in sanpodo, a tropomodulin actin-binding protein homologue, equalize a diverse array of sibling neuron fates (‘B/B’). Loss of Notch signaling gives the same phenotype, whereas loss 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 pathway. In addition, sanpodo and numb show dosage-sensitive interactions and epistasis experiments indicate that sanpodo acts downstream of numb. Taken together, these results show that interactions between sanpodo, the Notch signaling pathway and numb enable CNS sibling neurons to acquire different fates.