Zebrafish deadly seven functions in neurogenesis

In a genetic screen, we isolated a mutation that perturbed motor axon outgr owth, neurogenesis, and somitogenesis. Complementation tests revealed that this mutation is an allele of deadly seven (des). By creating genetic mosai cs, we demonstrate that the motor axon defect is non-cell autonomous. In ad dition, we show that the pattern of migration for some neural crest cell po pulations is aberrant and crest-derived dorsal root ganglion neurons are mi splaced. Furthermore, our analysis reveals that des mutant embryos exhibit a neurogenic phenotype. We find an increase in the number of primary motone urons and in the number of three hindbrain reticulospinal neurons: Mauthner cells, RoL2 cells, and MiD3cm cells. We also find that the number of Rohon -Beard sensory neurons is decreased whereas neural crest-derived dorsal roo t ganglion neurons are increased in number supporting a previous hypothesis that Rohon-Beard neurons and neural crest form an equivalence group during development. Mutations in genes involved in Notch-Delta signaling result i n defects in somitogenesis and neurogenesis. We found that overexpressing a n activated form of Notch decreased the number of Mauthner cells in des mut ants indicating that des functions via the Notch-Delta signaling pathway to control the production of specific cell types within the central and perip heral nervous systems. (C) 2001 Academic Press.